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Gene Information
Gene symbol: NOS1
Gene name: nitric oxide synthase 1 (neuronal)
HGNC ID: 7872
Synonyms: nNOS
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 7507509 | In addition, MRL-lpr/lpr peritoneal macrophages had an enhanced capacity to produce nitric oxide in vitro as well as increased nitric oxide synthase activity, and certain tissues from MRL-lpr/lpr mice had increased expression of inducible nitric oxide synthase (NOS) mRNA and increased amounts of material immunoreactive for inducible NOS. |
| 2 | 7507509 | However, the chromosomal location of the NOS gene was consistent with an insulin-dependent diabetes locus identified in an analysis of nonobese diabetic (NOD) mice. |
| 3 | 7507509 | In addition, MRL-lpr/lpr peritoneal macrophages had an enhanced capacity to produce nitric oxide in vitro as well as increased nitric oxide synthase activity, and certain tissues from MRL-lpr/lpr mice had increased expression of inducible nitric oxide synthase (NOS) mRNA and increased amounts of material immunoreactive for inducible NOS. |
| 4 | 7507509 | However, the chromosomal location of the NOS gene was consistent with an insulin-dependent diabetes locus identified in an analysis of nonobese diabetic (NOD) mice. |
| 5 | 7514568 | The similarity of sequence and cofactor binding sites has suggested that the NOS genes may also be related to cytochrome P450 reductase, as well as to plant and bacterial oxidoreductases. |
| 6 | 7514568 | Identification of the human gene for endothelial NOS (NOS3) was confirmed by nucleotide sequence analysis of the first coding exon, which was found to be identical to its cognate cDNA. |
| 7 | 7514568 | The similarity of sequence and cofactor binding sites has suggested that the NOS genes may also be related to cytochrome P450 reductase, as well as to plant and bacterial oxidoreductases. |
| 8 | 7514568 | Identification of the human gene for endothelial NOS (NOS3) was confirmed by nucleotide sequence analysis of the first coding exon, which was found to be identical to its cognate cDNA. |
| 9 | 7540553 | We tested the hypothesis that reduced NBF might be due to alterations of nitric oxide synthase (NOS) and endothelin of microvascular endothelial cells of sciatic nerve. |
| 10 | 7540553 | We applied the NOS inhibitor NG-nitro-L-arginine and observed reduced inhibition of NBF in EDN, correctable with insulin treatment and also with infused L-arginine. |
| 11 | 7540553 | Hyperglycemia is likely to be the mechanism of NOS inhibition since insulin treatment reversed this abnormality. |
| 12 | 7540553 | We tested the hypothesis that reduced NBF might be due to alterations of nitric oxide synthase (NOS) and endothelin of microvascular endothelial cells of sciatic nerve. |
| 13 | 7540553 | We applied the NOS inhibitor NG-nitro-L-arginine and observed reduced inhibition of NBF in EDN, correctable with insulin treatment and also with infused L-arginine. |
| 14 | 7540553 | Hyperglycemia is likely to be the mechanism of NOS inhibition since insulin treatment reversed this abnormality. |
| 15 | 7540553 | We tested the hypothesis that reduced NBF might be due to alterations of nitric oxide synthase (NOS) and endothelin of microvascular endothelial cells of sciatic nerve. |
| 16 | 7540553 | We applied the NOS inhibitor NG-nitro-L-arginine and observed reduced inhibition of NBF in EDN, correctable with insulin treatment and also with infused L-arginine. |
| 17 | 7540553 | Hyperglycemia is likely to be the mechanism of NOS inhibition since insulin treatment reversed this abnormality. |
| 18 | 7545787 | Pharmacological blockade of NO production with arginine analogues such as L-nitroarginine (L-NA) or L-N-arginine methyl ester affects multiple isoforms of nitric oxide synthase (NOS), and so cannot distinguish their physiological roles. |
| 19 | 7545787 | To study the role of endothelial NOS (eNOS) in vascular function, we disrupted the gene encoding eNOS in mice. |
| 20 | 7545787 | Pharmacological blockade of NO production with arginine analogues such as L-nitroarginine (L-NA) or L-N-arginine methyl ester affects multiple isoforms of nitric oxide synthase (NOS), and so cannot distinguish their physiological roles. |
| 21 | 7545787 | To study the role of endothelial NOS (eNOS) in vascular function, we disrupted the gene encoding eNOS in mice. |
| 22 | 7585335 | Selective type II (inducible) nitric oxide synthase (NOS) inhibitors have several potential therapeutic applications, including treatment of sepsis, diabetes, and autoimmune diseases. |
| 23 | 7588327 | It is also unknown whether diabetes-related impotence is due to reduced levels of the mediator of penile erection, nitric oxide, caused by a decrease of nitric oxide synthase (NOS) in the penis. |
| 24 | 8735786 | Increase in nitric oxide synthase and NADPH-diaphorase in the adrenal gland of streptozotocin-diabetic Wistar rats and its prevention by ganglioside. |
| 25 | 8735786 | Levels of nitric oxide synthase (NOS) and NADPH-diaphorase in adrenal glands of streptozotocin-diabetic rats of 8 and 12 weeks' duration compared with control rats were assessed with histo-chemical and biochemical techniques. |
| 26 | 8735786 | In the adrenal medulla of 8-weeks- and 12-weeks-diabetic rats, NOS-immunoreactive nerve fibres were increased and decreased, respectively; additional NOS-immunoreactive and NADPH-diaphorase stained cells, which appeared to be cortical cells, were located in medulla and cortex compared with controls. |
| 27 | 8735786 | Also, it reduced most of the increase in the NOS-immunoreactive and NADPH-diaphorase stained cells and the intensity of NADPH-diaphorase staining of cortical cells. |
| 28 | 8735786 | In summary, streptozotocin-induced diabetes causes an initial increase in the levels of NOS and NADPH-diaphorase in the adrenal gland of rat, which was prevented by ganglioside treatment. |
| 29 | 8735786 | Increase in nitric oxide synthase and NADPH-diaphorase in the adrenal gland of streptozotocin-diabetic Wistar rats and its prevention by ganglioside. |
| 30 | 8735786 | Levels of nitric oxide synthase (NOS) and NADPH-diaphorase in adrenal glands of streptozotocin-diabetic rats of 8 and 12 weeks' duration compared with control rats were assessed with histo-chemical and biochemical techniques. |
| 31 | 8735786 | In the adrenal medulla of 8-weeks- and 12-weeks-diabetic rats, NOS-immunoreactive nerve fibres were increased and decreased, respectively; additional NOS-immunoreactive and NADPH-diaphorase stained cells, which appeared to be cortical cells, were located in medulla and cortex compared with controls. |
| 32 | 8735786 | Also, it reduced most of the increase in the NOS-immunoreactive and NADPH-diaphorase stained cells and the intensity of NADPH-diaphorase staining of cortical cells. |
| 33 | 8735786 | In summary, streptozotocin-induced diabetes causes an initial increase in the levels of NOS and NADPH-diaphorase in the adrenal gland of rat, which was prevented by ganglioside treatment. |
| 34 | 8735786 | Increase in nitric oxide synthase and NADPH-diaphorase in the adrenal gland of streptozotocin-diabetic Wistar rats and its prevention by ganglioside. |
| 35 | 8735786 | Levels of nitric oxide synthase (NOS) and NADPH-diaphorase in adrenal glands of streptozotocin-diabetic rats of 8 and 12 weeks' duration compared with control rats were assessed with histo-chemical and biochemical techniques. |
| 36 | 8735786 | In the adrenal medulla of 8-weeks- and 12-weeks-diabetic rats, NOS-immunoreactive nerve fibres were increased and decreased, respectively; additional NOS-immunoreactive and NADPH-diaphorase stained cells, which appeared to be cortical cells, were located in medulla and cortex compared with controls. |
| 37 | 8735786 | Also, it reduced most of the increase in the NOS-immunoreactive and NADPH-diaphorase stained cells and the intensity of NADPH-diaphorase staining of cortical cells. |
| 38 | 8735786 | In summary, streptozotocin-induced diabetes causes an initial increase in the levels of NOS and NADPH-diaphorase in the adrenal gland of rat, which was prevented by ganglioside treatment. |
| 39 | 8735786 | Increase in nitric oxide synthase and NADPH-diaphorase in the adrenal gland of streptozotocin-diabetic Wistar rats and its prevention by ganglioside. |
| 40 | 8735786 | Levels of nitric oxide synthase (NOS) and NADPH-diaphorase in adrenal glands of streptozotocin-diabetic rats of 8 and 12 weeks' duration compared with control rats were assessed with histo-chemical and biochemical techniques. |
| 41 | 8735786 | In the adrenal medulla of 8-weeks- and 12-weeks-diabetic rats, NOS-immunoreactive nerve fibres were increased and decreased, respectively; additional NOS-immunoreactive and NADPH-diaphorase stained cells, which appeared to be cortical cells, were located in medulla and cortex compared with controls. |
| 42 | 8735786 | Also, it reduced most of the increase in the NOS-immunoreactive and NADPH-diaphorase stained cells and the intensity of NADPH-diaphorase staining of cortical cells. |
| 43 | 8735786 | In summary, streptozotocin-induced diabetes causes an initial increase in the levels of NOS and NADPH-diaphorase in the adrenal gland of rat, which was prevented by ganglioside treatment. |
| 44 | 8750048 | This article outlines the identification of numerous nitric oxide synthase (NOS) and VIP-containing axons in the human penis. |
| 45 | 8770936 | It has also been shown that diabetes-induced inactivation of NO can be rescued with administration of insulin as well as with free radical scavengers such as superoxide dismutase (SOD). |
| 46 | 8770936 | Lastly, we report the localization of endothelial nitric oxide synthase, inducible NOS, Cu/Zn SOD, and the LH receptor to the same population of endothelial cells surrounding the preovulatory follicle, supporting our hypothesis that the signaling of ovarian NO within the ovarian microvasculature at the time of ovulation may be compromised in these diabetic mice as a consequence of the loss of the protective activity of Cu/Zn SOD. |
| 47 | 8779862 | Roles of IL-1 and TNF-alpha in endotoxin-induced activation of nitric oxide synthase in cultured rat brain cells. |
| 48 | 8779862 | In astrocytes and microglia, bacterial lipopolysaccharide (LPS) stimulates production and release of interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), and nitric oxide (NO). |
| 49 | 8779862 | Although IL-1 beta and TNF-alpha are themselves capable of inducing NO synthase (NOS) in glia, the specific factors mediating LPS induction of NOS in brain have not been identified. |
| 50 | 8779862 | To determine whether LPS induction of NOS in brain cells is mediated by IL-1 or TNF-alpha, acting alone or in concert, the effects of IL-1-receptor antagonist (IL-1Ra) and of TNF-soluble receptor (TNFsRp55), presented individually and in combination, on LPS-induced NOS activity were tested. |
| 51 | 8779862 | In glial-enriched mixed primary cultures of neonatal rat telencephalic cells, LPS (0.1-100 ng/ml), IL-1 beta (0.01-10 nM), and TNF-alpha (0.1-100 nM) each concentration dependently stimulated accumulation of nitrite, an indicator of NO production. |
| 52 | 8779862 | Induction of nitrite accumulation by LPS and by IL-1 was blocked by N omega-nitro-L-arginine methyl ester and N omega-monomethyl-L-arginine, indicating that it was mediated by NOS. |
| 53 | 8779862 | TNF-alpha alone induced NO production weakly as compared with IL-1, but combined submaximal concentrations of IL-1 beta (1 nM) and TNF-alpha (10 nM) induced NOS synergistically. |
| 54 | 8779862 | The results indicate that LPS induction of NOS activity in brain cells is mediated in part by both IL-1 beta and TNF-alpha. |
| 55 | 8779862 | Roles of IL-1 and TNF-alpha in endotoxin-induced activation of nitric oxide synthase in cultured rat brain cells. |
| 56 | 8779862 | In astrocytes and microglia, bacterial lipopolysaccharide (LPS) stimulates production and release of interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), and nitric oxide (NO). |
| 57 | 8779862 | Although IL-1 beta and TNF-alpha are themselves capable of inducing NO synthase (NOS) in glia, the specific factors mediating LPS induction of NOS in brain have not been identified. |
| 58 | 8779862 | To determine whether LPS induction of NOS in brain cells is mediated by IL-1 or TNF-alpha, acting alone or in concert, the effects of IL-1-receptor antagonist (IL-1Ra) and of TNF-soluble receptor (TNFsRp55), presented individually and in combination, on LPS-induced NOS activity were tested. |
| 59 | 8779862 | In glial-enriched mixed primary cultures of neonatal rat telencephalic cells, LPS (0.1-100 ng/ml), IL-1 beta (0.01-10 nM), and TNF-alpha (0.1-100 nM) each concentration dependently stimulated accumulation of nitrite, an indicator of NO production. |
| 60 | 8779862 | Induction of nitrite accumulation by LPS and by IL-1 was blocked by N omega-nitro-L-arginine methyl ester and N omega-monomethyl-L-arginine, indicating that it was mediated by NOS. |
| 61 | 8779862 | TNF-alpha alone induced NO production weakly as compared with IL-1, but combined submaximal concentrations of IL-1 beta (1 nM) and TNF-alpha (10 nM) induced NOS synergistically. |
| 62 | 8779862 | The results indicate that LPS induction of NOS activity in brain cells is mediated in part by both IL-1 beta and TNF-alpha. |
| 63 | 8779862 | Roles of IL-1 and TNF-alpha in endotoxin-induced activation of nitric oxide synthase in cultured rat brain cells. |
| 64 | 8779862 | In astrocytes and microglia, bacterial lipopolysaccharide (LPS) stimulates production and release of interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), and nitric oxide (NO). |
| 65 | 8779862 | Although IL-1 beta and TNF-alpha are themselves capable of inducing NO synthase (NOS) in glia, the specific factors mediating LPS induction of NOS in brain have not been identified. |
| 66 | 8779862 | To determine whether LPS induction of NOS in brain cells is mediated by IL-1 or TNF-alpha, acting alone or in concert, the effects of IL-1-receptor antagonist (IL-1Ra) and of TNF-soluble receptor (TNFsRp55), presented individually and in combination, on LPS-induced NOS activity were tested. |
| 67 | 8779862 | In glial-enriched mixed primary cultures of neonatal rat telencephalic cells, LPS (0.1-100 ng/ml), IL-1 beta (0.01-10 nM), and TNF-alpha (0.1-100 nM) each concentration dependently stimulated accumulation of nitrite, an indicator of NO production. |
| 68 | 8779862 | Induction of nitrite accumulation by LPS and by IL-1 was blocked by N omega-nitro-L-arginine methyl ester and N omega-monomethyl-L-arginine, indicating that it was mediated by NOS. |
| 69 | 8779862 | TNF-alpha alone induced NO production weakly as compared with IL-1, but combined submaximal concentrations of IL-1 beta (1 nM) and TNF-alpha (10 nM) induced NOS synergistically. |
| 70 | 8779862 | The results indicate that LPS induction of NOS activity in brain cells is mediated in part by both IL-1 beta and TNF-alpha. |
| 71 | 8779862 | Roles of IL-1 and TNF-alpha in endotoxin-induced activation of nitric oxide synthase in cultured rat brain cells. |
| 72 | 8779862 | In astrocytes and microglia, bacterial lipopolysaccharide (LPS) stimulates production and release of interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), and nitric oxide (NO). |
| 73 | 8779862 | Although IL-1 beta and TNF-alpha are themselves capable of inducing NO synthase (NOS) in glia, the specific factors mediating LPS induction of NOS in brain have not been identified. |
| 74 | 8779862 | To determine whether LPS induction of NOS in brain cells is mediated by IL-1 or TNF-alpha, acting alone or in concert, the effects of IL-1-receptor antagonist (IL-1Ra) and of TNF-soluble receptor (TNFsRp55), presented individually and in combination, on LPS-induced NOS activity were tested. |
| 75 | 8779862 | In glial-enriched mixed primary cultures of neonatal rat telencephalic cells, LPS (0.1-100 ng/ml), IL-1 beta (0.01-10 nM), and TNF-alpha (0.1-100 nM) each concentration dependently stimulated accumulation of nitrite, an indicator of NO production. |
| 76 | 8779862 | Induction of nitrite accumulation by LPS and by IL-1 was blocked by N omega-nitro-L-arginine methyl ester and N omega-monomethyl-L-arginine, indicating that it was mediated by NOS. |
| 77 | 8779862 | TNF-alpha alone induced NO production weakly as compared with IL-1, but combined submaximal concentrations of IL-1 beta (1 nM) and TNF-alpha (10 nM) induced NOS synergistically. |
| 78 | 8779862 | The results indicate that LPS induction of NOS activity in brain cells is mediated in part by both IL-1 beta and TNF-alpha. |
| 79 | 8779862 | Roles of IL-1 and TNF-alpha in endotoxin-induced activation of nitric oxide synthase in cultured rat brain cells. |
| 80 | 8779862 | In astrocytes and microglia, bacterial lipopolysaccharide (LPS) stimulates production and release of interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), and nitric oxide (NO). |
| 81 | 8779862 | Although IL-1 beta and TNF-alpha are themselves capable of inducing NO synthase (NOS) in glia, the specific factors mediating LPS induction of NOS in brain have not been identified. |
| 82 | 8779862 | To determine whether LPS induction of NOS in brain cells is mediated by IL-1 or TNF-alpha, acting alone or in concert, the effects of IL-1-receptor antagonist (IL-1Ra) and of TNF-soluble receptor (TNFsRp55), presented individually and in combination, on LPS-induced NOS activity were tested. |
| 83 | 8779862 | In glial-enriched mixed primary cultures of neonatal rat telencephalic cells, LPS (0.1-100 ng/ml), IL-1 beta (0.01-10 nM), and TNF-alpha (0.1-100 nM) each concentration dependently stimulated accumulation of nitrite, an indicator of NO production. |
| 84 | 8779862 | Induction of nitrite accumulation by LPS and by IL-1 was blocked by N omega-nitro-L-arginine methyl ester and N omega-monomethyl-L-arginine, indicating that it was mediated by NOS. |
| 85 | 8779862 | TNF-alpha alone induced NO production weakly as compared with IL-1, but combined submaximal concentrations of IL-1 beta (1 nM) and TNF-alpha (10 nM) induced NOS synergistically. |
| 86 | 8779862 | The results indicate that LPS induction of NOS activity in brain cells is mediated in part by both IL-1 beta and TNF-alpha. |
| 87 | 8817103 | This study was therefore designed to clarify whether in situ expression of nitric oxide synthase (NOS) is altered in the kidney of diabetic rats. |
| 88 | 8817103 | The expression of a constitutive form of NOS (cNOS, neural type) and NADPH diaphorase activity in the renal cortex were studied immunohistochemically and histochemically. |
| 89 | 8817103 | This study was therefore designed to clarify whether in situ expression of nitric oxide synthase (NOS) is altered in the kidney of diabetic rats. |
| 90 | 8817103 | The expression of a constitutive form of NOS (cNOS, neural type) and NADPH diaphorase activity in the renal cortex were studied immunohistochemically and histochemically. |
| 91 | 9000650 | Aldose reductase and nitric oxide synthase(NOS) share NADPH as an obligate cofactor, therefore it is suggested that the enhanced of glucose flux (27.5 mM) by aldose reductase inhibited NO production by blunting NOS activity. |
| 92 | 9029239 | Nitric oxide synthase (NOS) is expressed in skeletal muscle. |
| 93 | 9029239 | To determine the role of NO in modulating glucose transport, 2-deoxyglucose (2-DG) transport was measured in rat extensor digitorum longus (EDL) muscles that were exposed to either a maximally stimulating concentration of insulin or to an electrical stimulation protocol, in the presence of NG-monomethyl-L-arginine, a NOS inhibitor. |
| 94 | 9029239 | NOS inhibition reduced both basal and exercise-enhanced 2-DG transport but had no effect on insulin-stimulated 2-DG transport. |
| 95 | 9029239 | Nitric oxide synthase (NOS) is expressed in skeletal muscle. |
| 96 | 9029239 | To determine the role of NO in modulating glucose transport, 2-deoxyglucose (2-DG) transport was measured in rat extensor digitorum longus (EDL) muscles that were exposed to either a maximally stimulating concentration of insulin or to an electrical stimulation protocol, in the presence of NG-monomethyl-L-arginine, a NOS inhibitor. |
| 97 | 9029239 | NOS inhibition reduced both basal and exercise-enhanced 2-DG transport but had no effect on insulin-stimulated 2-DG transport. |
| 98 | 9029239 | Nitric oxide synthase (NOS) is expressed in skeletal muscle. |
| 99 | 9029239 | To determine the role of NO in modulating glucose transport, 2-deoxyglucose (2-DG) transport was measured in rat extensor digitorum longus (EDL) muscles that were exposed to either a maximally stimulating concentration of insulin or to an electrical stimulation protocol, in the presence of NG-monomethyl-L-arginine, a NOS inhibitor. |
| 100 | 9029239 | NOS inhibition reduced both basal and exercise-enhanced 2-DG transport but had no effect on insulin-stimulated 2-DG transport. |
| 101 | 9171957 | To investigate the role of nitric oxide (NO) in diabetic nephropathy the effect of nitric oxide synthase (NOS) inhibition by NG-nitro-L-arginine methyl ester (L-NAME) was observed in a streptozotocin diabetic spontaneously hypertensive rat (SHR) model. 2. |
| 102 | 9299363 | Left ventricular performance was measured in isolated working hearts, before and at the peak response to 0.8 microM dobutamine, in the absence or presence of NG-nitro-L-arginine methyl ester (L-NAME, 1 mM), a non-selective inhibitor of nitric oxide synthase (NOS). |
| 103 | 9299363 | Western blot analysis detected the presence of inducible nitric oxide synthase (NOS) and a significant (P<0.001) increase in the constitutive NOS in ventricular myocytes from STZ-Db rats. |
| 104 | 9299363 | Left ventricular performance was measured in isolated working hearts, before and at the peak response to 0.8 microM dobutamine, in the absence or presence of NG-nitro-L-arginine methyl ester (L-NAME, 1 mM), a non-selective inhibitor of nitric oxide synthase (NOS). |
| 105 | 9299363 | Western blot analysis detected the presence of inducible nitric oxide synthase (NOS) and a significant (P<0.001) increase in the constitutive NOS in ventricular myocytes from STZ-Db rats. |
| 106 | 9356014 | Expression of nitric oxide synthase in skeletal muscle: a novel role for nitric oxide as a modulator of insulin action. |
| 107 | 9356014 | Previous studies have shown that nitric oxide synthase (NOS), the enzyme that catalyzes the formation of nitric oxide (NO), is expressed in skeletal muscle. |
| 108 | 9356014 | Both the neuronal-type (nNOS) and endothelial-type (eNOS) enzymes are expressed in resting skeletal muscles. |
| 109 | 9356014 | However, nNOS protein was only detected in EDL muscles, whereas eNOS protein contents were comparable in soleus and EDL muscles. |
| 110 | 9356014 | NOS expression in muscle cryosections (diaphorase histochemistry) was located in vascular endothelium and in muscle fibers, and the staining was greater in type IIb than in type I and IIa fibers. |
| 111 | 9356014 | The macrophage-type inducible NOS (iNOS) was not detected in resting muscle, but endotoxin treatment induced its expression, concomitant with elevated NO production. iNOS induction was associated with impaired insulin-stimulated glucose uptake in isolated rat muscles. |
| 112 | 9356014 | In vitro, NOS blockade with specific inhibitors did not affect basal or insulin-stimulated glucose transport in EDL or soleus muscles. |
| 113 | 9356014 | Expression of nitric oxide synthase in skeletal muscle: a novel role for nitric oxide as a modulator of insulin action. |
| 114 | 9356014 | Previous studies have shown that nitric oxide synthase (NOS), the enzyme that catalyzes the formation of nitric oxide (NO), is expressed in skeletal muscle. |
| 115 | 9356014 | Both the neuronal-type (nNOS) and endothelial-type (eNOS) enzymes are expressed in resting skeletal muscles. |
| 116 | 9356014 | However, nNOS protein was only detected in EDL muscles, whereas eNOS protein contents were comparable in soleus and EDL muscles. |
| 117 | 9356014 | NOS expression in muscle cryosections (diaphorase histochemistry) was located in vascular endothelium and in muscle fibers, and the staining was greater in type IIb than in type I and IIa fibers. |
| 118 | 9356014 | The macrophage-type inducible NOS (iNOS) was not detected in resting muscle, but endotoxin treatment induced its expression, concomitant with elevated NO production. iNOS induction was associated with impaired insulin-stimulated glucose uptake in isolated rat muscles. |
| 119 | 9356014 | In vitro, NOS blockade with specific inhibitors did not affect basal or insulin-stimulated glucose transport in EDL or soleus muscles. |
| 120 | 9356014 | Expression of nitric oxide synthase in skeletal muscle: a novel role for nitric oxide as a modulator of insulin action. |
| 121 | 9356014 | Previous studies have shown that nitric oxide synthase (NOS), the enzyme that catalyzes the formation of nitric oxide (NO), is expressed in skeletal muscle. |
| 122 | 9356014 | Both the neuronal-type (nNOS) and endothelial-type (eNOS) enzymes are expressed in resting skeletal muscles. |
| 123 | 9356014 | However, nNOS protein was only detected in EDL muscles, whereas eNOS protein contents were comparable in soleus and EDL muscles. |
| 124 | 9356014 | NOS expression in muscle cryosections (diaphorase histochemistry) was located in vascular endothelium and in muscle fibers, and the staining was greater in type IIb than in type I and IIa fibers. |
| 125 | 9356014 | The macrophage-type inducible NOS (iNOS) was not detected in resting muscle, but endotoxin treatment induced its expression, concomitant with elevated NO production. iNOS induction was associated with impaired insulin-stimulated glucose uptake in isolated rat muscles. |
| 126 | 9356014 | In vitro, NOS blockade with specific inhibitors did not affect basal or insulin-stimulated glucose transport in EDL or soleus muscles. |
| 127 | 9356014 | Expression of nitric oxide synthase in skeletal muscle: a novel role for nitric oxide as a modulator of insulin action. |
| 128 | 9356014 | Previous studies have shown that nitric oxide synthase (NOS), the enzyme that catalyzes the formation of nitric oxide (NO), is expressed in skeletal muscle. |
| 129 | 9356014 | Both the neuronal-type (nNOS) and endothelial-type (eNOS) enzymes are expressed in resting skeletal muscles. |
| 130 | 9356014 | However, nNOS protein was only detected in EDL muscles, whereas eNOS protein contents were comparable in soleus and EDL muscles. |
| 131 | 9356014 | NOS expression in muscle cryosections (diaphorase histochemistry) was located in vascular endothelium and in muscle fibers, and the staining was greater in type IIb than in type I and IIa fibers. |
| 132 | 9356014 | The macrophage-type inducible NOS (iNOS) was not detected in resting muscle, but endotoxin treatment induced its expression, concomitant with elevated NO production. iNOS induction was associated with impaired insulin-stimulated glucose uptake in isolated rat muscles. |
| 133 | 9356014 | In vitro, NOS blockade with specific inhibitors did not affect basal or insulin-stimulated glucose transport in EDL or soleus muscles. |
| 134 | 9356014 | Expression of nitric oxide synthase in skeletal muscle: a novel role for nitric oxide as a modulator of insulin action. |
| 135 | 9356014 | Previous studies have shown that nitric oxide synthase (NOS), the enzyme that catalyzes the formation of nitric oxide (NO), is expressed in skeletal muscle. |
| 136 | 9356014 | Both the neuronal-type (nNOS) and endothelial-type (eNOS) enzymes are expressed in resting skeletal muscles. |
| 137 | 9356014 | However, nNOS protein was only detected in EDL muscles, whereas eNOS protein contents were comparable in soleus and EDL muscles. |
| 138 | 9356014 | NOS expression in muscle cryosections (diaphorase histochemistry) was located in vascular endothelium and in muscle fibers, and the staining was greater in type IIb than in type I and IIa fibers. |
| 139 | 9356014 | The macrophage-type inducible NOS (iNOS) was not detected in resting muscle, but endotoxin treatment induced its expression, concomitant with elevated NO production. iNOS induction was associated with impaired insulin-stimulated glucose uptake in isolated rat muscles. |
| 140 | 9356014 | In vitro, NOS blockade with specific inhibitors did not affect basal or insulin-stimulated glucose transport in EDL or soleus muscles. |
| 141 | 9356014 | Expression of nitric oxide synthase in skeletal muscle: a novel role for nitric oxide as a modulator of insulin action. |
| 142 | 9356014 | Previous studies have shown that nitric oxide synthase (NOS), the enzyme that catalyzes the formation of nitric oxide (NO), is expressed in skeletal muscle. |
| 143 | 9356014 | Both the neuronal-type (nNOS) and endothelial-type (eNOS) enzymes are expressed in resting skeletal muscles. |
| 144 | 9356014 | However, nNOS protein was only detected in EDL muscles, whereas eNOS protein contents were comparable in soleus and EDL muscles. |
| 145 | 9356014 | NOS expression in muscle cryosections (diaphorase histochemistry) was located in vascular endothelium and in muscle fibers, and the staining was greater in type IIb than in type I and IIa fibers. |
| 146 | 9356014 | The macrophage-type inducible NOS (iNOS) was not detected in resting muscle, but endotoxin treatment induced its expression, concomitant with elevated NO production. iNOS induction was associated with impaired insulin-stimulated glucose uptake in isolated rat muscles. |
| 147 | 9356014 | In vitro, NOS blockade with specific inhibitors did not affect basal or insulin-stimulated glucose transport in EDL or soleus muscles. |
| 148 | 9365143 | Nitric oxide synthase (NOS) expression in the myenteric plexus of streptozotocin-diabetic rats. |
| 149 | 9365143 | The presence of nitric oxide synthase (NOS) reflects the potential for NO synthesis and is found in neurons in the myenteric plexus. |
| 150 | 9365143 | The aim of this study was to determine changes in nitric oxide synthase (NOS) expression in the myenteric plexus of the gastrointestinal tract of diabetic rats at three months of streptozotocin-induced diabetes, compared to age matched controls, using immunohistochemistry. |
| 151 | 9365143 | Nitric oxide synthase (NOS) expression in the myenteric plexus of streptozotocin-diabetic rats. |
| 152 | 9365143 | The presence of nitric oxide synthase (NOS) reflects the potential for NO synthesis and is found in neurons in the myenteric plexus. |
| 153 | 9365143 | The aim of this study was to determine changes in nitric oxide synthase (NOS) expression in the myenteric plexus of the gastrointestinal tract of diabetic rats at three months of streptozotocin-induced diabetes, compared to age matched controls, using immunohistochemistry. |
| 154 | 9365143 | Nitric oxide synthase (NOS) expression in the myenteric plexus of streptozotocin-diabetic rats. |
| 155 | 9365143 | The presence of nitric oxide synthase (NOS) reflects the potential for NO synthesis and is found in neurons in the myenteric plexus. |
| 156 | 9365143 | The aim of this study was to determine changes in nitric oxide synthase (NOS) expression in the myenteric plexus of the gastrointestinal tract of diabetic rats at three months of streptozotocin-induced diabetes, compared to age matched controls, using immunohistochemistry. |
| 157 | 9453318 | Calcium and protein kinase C mediate high-glucose-induced inhibition of inducible nitric oxide synthase in vascular smooth muscle cells. |
| 158 | 9453318 | IL-1beta-stimulated [3H] citrulline-forming activity of the nitric oxide synthase (NOS) was also significantly lower in high-glucose-exposed cells, and this was reflected in diminished cellular levels of NOS protein. |
| 159 | 9462464 | Upregulation of neuronal NOS mRNA in the PVN and SON of inherited diabetes insipidus rats. |
| 160 | 9462464 | We investigated the expression of neuronal nitric oxide synthase (nNOS) gene in the paraventricular (PVN) and supraoptic nuclei (SON) of rats with inherited diabetes insipidus (DI), using in situ hybridization histochemistry. |
| 161 | 9462464 | The expression of nNOS gene in the PVN and SON in homozygous (di/di) rats was significantly increased in comparison to normal Wistar and heterozygous (di/+) rats. nNOS gene-expressing cells were distributed throughout the PVN and SON, including the divisions of AVP and oxytocin gene expressing cells in di/di rats. |
| 162 | 9462464 | These results suggest that the expression of nNOS gene is upregulated in the magnocellular neurons in the PVN and SON of inherited DI rats. |
| 163 | 9462464 | Upregulation of neuronal NOS mRNA in the PVN and SON of inherited diabetes insipidus rats. |
| 164 | 9462464 | We investigated the expression of neuronal nitric oxide synthase (nNOS) gene in the paraventricular (PVN) and supraoptic nuclei (SON) of rats with inherited diabetes insipidus (DI), using in situ hybridization histochemistry. |
| 165 | 9462464 | The expression of nNOS gene in the PVN and SON in homozygous (di/di) rats was significantly increased in comparison to normal Wistar and heterozygous (di/+) rats. nNOS gene-expressing cells were distributed throughout the PVN and SON, including the divisions of AVP and oxytocin gene expressing cells in di/di rats. |
| 166 | 9462464 | These results suggest that the expression of nNOS gene is upregulated in the magnocellular neurons in the PVN and SON of inherited DI rats. |
| 167 | 9462464 | Upregulation of neuronal NOS mRNA in the PVN and SON of inherited diabetes insipidus rats. |
| 168 | 9462464 | We investigated the expression of neuronal nitric oxide synthase (nNOS) gene in the paraventricular (PVN) and supraoptic nuclei (SON) of rats with inherited diabetes insipidus (DI), using in situ hybridization histochemistry. |
| 169 | 9462464 | The expression of nNOS gene in the PVN and SON in homozygous (di/di) rats was significantly increased in comparison to normal Wistar and heterozygous (di/+) rats. nNOS gene-expressing cells were distributed throughout the PVN and SON, including the divisions of AVP and oxytocin gene expressing cells in di/di rats. |
| 170 | 9462464 | These results suggest that the expression of nNOS gene is upregulated in the magnocellular neurons in the PVN and SON of inherited DI rats. |
| 171 | 9462464 | Upregulation of neuronal NOS mRNA in the PVN and SON of inherited diabetes insipidus rats. |
| 172 | 9462464 | We investigated the expression of neuronal nitric oxide synthase (nNOS) gene in the paraventricular (PVN) and supraoptic nuclei (SON) of rats with inherited diabetes insipidus (DI), using in situ hybridization histochemistry. |
| 173 | 9462464 | The expression of nNOS gene in the PVN and SON in homozygous (di/di) rats was significantly increased in comparison to normal Wistar and heterozygous (di/+) rats. nNOS gene-expressing cells were distributed throughout the PVN and SON, including the divisions of AVP and oxytocin gene expressing cells in di/di rats. |
| 174 | 9462464 | These results suggest that the expression of nNOS gene is upregulated in the magnocellular neurons in the PVN and SON of inherited DI rats. |
| 175 | 9498637 | Decreased nitric oxide synthase activity in platelets from IDDM and NIDDM patients. |
| 176 | 9498637 | Nitric oxide (NO) produced by platelet nitric oxide synthase (NOS) inhibits platelet activation by increased cytoplasmic cGMP levels. |
| 177 | 9498637 | The aim of this study was to investigate platelet NOS activity in insulin-dependent (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM), which are characterized by enhanced platelet activation. |
| 178 | 9498637 | HbA1c levels, platelet NOS and platelet membrane Na+/K+ ATPase activity were determined in 19 IDDM patients, 21 NIDDM patients and 31 healthy control subjects. |
| 179 | 9498637 | Decreased nitric oxide synthase activity in platelets from IDDM and NIDDM patients. |
| 180 | 9498637 | Nitric oxide (NO) produced by platelet nitric oxide synthase (NOS) inhibits platelet activation by increased cytoplasmic cGMP levels. |
| 181 | 9498637 | The aim of this study was to investigate platelet NOS activity in insulin-dependent (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM), which are characterized by enhanced platelet activation. |
| 182 | 9498637 | HbA1c levels, platelet NOS and platelet membrane Na+/K+ ATPase activity were determined in 19 IDDM patients, 21 NIDDM patients and 31 healthy control subjects. |
| 183 | 9498637 | Decreased nitric oxide synthase activity in platelets from IDDM and NIDDM patients. |
| 184 | 9498637 | Nitric oxide (NO) produced by platelet nitric oxide synthase (NOS) inhibits platelet activation by increased cytoplasmic cGMP levels. |
| 185 | 9498637 | The aim of this study was to investigate platelet NOS activity in insulin-dependent (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM), which are characterized by enhanced platelet activation. |
| 186 | 9498637 | HbA1c levels, platelet NOS and platelet membrane Na+/K+ ATPase activity were determined in 19 IDDM patients, 21 NIDDM patients and 31 healthy control subjects. |
| 187 | 9507963 | To evaluate the role of nitric oxide synthase (nNOS) in the pathogenesis of diabetic neuropathy, we investigated nociception and nNOS expression in dorsal root ganglion (DRG) of rats with streptozocin-induced diabetes. |
| 188 | 9507963 | Insulin treatment completely prevented decreases in withdrawal threshold and nNOS expression. |
| 189 | 9507963 | To evaluate the role of nitric oxide synthase (nNOS) in the pathogenesis of diabetic neuropathy, we investigated nociception and nNOS expression in dorsal root ganglion (DRG) of rats with streptozocin-induced diabetes. |
| 190 | 9507963 | Insulin treatment completely prevented decreases in withdrawal threshold and nNOS expression. |
| 191 | 9510080 | Nitric oxide synthase (NOS) activity was studied in the retinas from normal rats and in the retinas from two groups of streptozotocin-induced (8 days and 4 months) diabetic rats. |
| 192 | 9604873 | The expression of vascular endothelial constitutive nitric oxide synthase (eNOS), which is responsible for NO synthesis in endothelial cells, was studied by Western blot analysis and Northern hybridization experiments. |
| 193 | 9604873 | This study also suggests that glycated proteins may be involved in the pathogenesis of vascular endothelial dysfunction by modulating the nitric oxide synthase (NOS)/NO pathway in retinal vascular endothelial cells. |
| 194 | 9641554 | The nitric oxide synthase (NOS) inhibitor (L-NAME; 0.3, 1 or 3 mg ml(-1), p.o.) when administered in vivo increased blood pressure in cp/cp rats but not in +/? |
| 195 | 9662044 | Plasma arginine vasopressin (AVP) is known to be elevated in patients with uncontrolled insulin-dependent diabetes mellitus who have plasma hyperosmolality with hyperglycaemia. |
| 196 | 9662044 | Although osmotic stimuli cause an increase in nitric oxide synthase (NOS) activity as well as synthesis of AVP and oxytocin in the paraventricular (PVN) and supraoptic nuclei (SON), it is not known whether NOS activity in the hypothalamus changes in the diabetic patients who have plasma hyperosmolality with hyperglycaemia caused by insulin deficiency. |
| 197 | 9662044 | Expression of the neuronal (n) NOS gene in the PVN and SON in streptozotocin (STZ)-induced diabetic rats was investigated by using in situ hybridization histochemistry and NADPH-diaphorase histochemical staining. |
| 198 | 9662044 | The expression of nNOS gene and NADPH-diaphorase staining in the PVN and SON remarkably increased in STZ-induced diabetic rats compared to control rats. |
| 199 | 9662044 | Three weeks after administration of STZ, the diabetic rats were subcutaneously treated with insulin for 1 week, which resulted in significant suppression of the induction of nNOS, AVP and oxytocin gene expression in the PVN and SON. |
| 200 | 9662044 | Furthermore, the induction of nNOS gene expression in the PVN and SON was suppressed in STZ-induced diabetic rats treated with phlorizin and diet to normalize hyperglycaemia without insulin treatment. |
| 201 | 9662044 | These results suggest that upregulation of nNOS gene expression as well as AVP and oxytocin gene expression in the PVN and SON in STZ-induced diabetic rats may be associated with hyperglycaemia and plamsa hyperosmolality. |
| 202 | 9662044 | Plasma arginine vasopressin (AVP) is known to be elevated in patients with uncontrolled insulin-dependent diabetes mellitus who have plasma hyperosmolality with hyperglycaemia. |
| 203 | 9662044 | Although osmotic stimuli cause an increase in nitric oxide synthase (NOS) activity as well as synthesis of AVP and oxytocin in the paraventricular (PVN) and supraoptic nuclei (SON), it is not known whether NOS activity in the hypothalamus changes in the diabetic patients who have plasma hyperosmolality with hyperglycaemia caused by insulin deficiency. |
| 204 | 9662044 | Expression of the neuronal (n) NOS gene in the PVN and SON in streptozotocin (STZ)-induced diabetic rats was investigated by using in situ hybridization histochemistry and NADPH-diaphorase histochemical staining. |
| 205 | 9662044 | The expression of nNOS gene and NADPH-diaphorase staining in the PVN and SON remarkably increased in STZ-induced diabetic rats compared to control rats. |
| 206 | 9662044 | Three weeks after administration of STZ, the diabetic rats were subcutaneously treated with insulin for 1 week, which resulted in significant suppression of the induction of nNOS, AVP and oxytocin gene expression in the PVN and SON. |
| 207 | 9662044 | Furthermore, the induction of nNOS gene expression in the PVN and SON was suppressed in STZ-induced diabetic rats treated with phlorizin and diet to normalize hyperglycaemia without insulin treatment. |
| 208 | 9662044 | These results suggest that upregulation of nNOS gene expression as well as AVP and oxytocin gene expression in the PVN and SON in STZ-induced diabetic rats may be associated with hyperglycaemia and plamsa hyperosmolality. |
| 209 | 9662044 | Plasma arginine vasopressin (AVP) is known to be elevated in patients with uncontrolled insulin-dependent diabetes mellitus who have plasma hyperosmolality with hyperglycaemia. |
| 210 | 9662044 | Although osmotic stimuli cause an increase in nitric oxide synthase (NOS) activity as well as synthesis of AVP and oxytocin in the paraventricular (PVN) and supraoptic nuclei (SON), it is not known whether NOS activity in the hypothalamus changes in the diabetic patients who have plasma hyperosmolality with hyperglycaemia caused by insulin deficiency. |
| 211 | 9662044 | Expression of the neuronal (n) NOS gene in the PVN and SON in streptozotocin (STZ)-induced diabetic rats was investigated by using in situ hybridization histochemistry and NADPH-diaphorase histochemical staining. |
| 212 | 9662044 | The expression of nNOS gene and NADPH-diaphorase staining in the PVN and SON remarkably increased in STZ-induced diabetic rats compared to control rats. |
| 213 | 9662044 | Three weeks after administration of STZ, the diabetic rats were subcutaneously treated with insulin for 1 week, which resulted in significant suppression of the induction of nNOS, AVP and oxytocin gene expression in the PVN and SON. |
| 214 | 9662044 | Furthermore, the induction of nNOS gene expression in the PVN and SON was suppressed in STZ-induced diabetic rats treated with phlorizin and diet to normalize hyperglycaemia without insulin treatment. |
| 215 | 9662044 | These results suggest that upregulation of nNOS gene expression as well as AVP and oxytocin gene expression in the PVN and SON in STZ-induced diabetic rats may be associated with hyperglycaemia and plamsa hyperosmolality. |
| 216 | 9662044 | Plasma arginine vasopressin (AVP) is known to be elevated in patients with uncontrolled insulin-dependent diabetes mellitus who have plasma hyperosmolality with hyperglycaemia. |
| 217 | 9662044 | Although osmotic stimuli cause an increase in nitric oxide synthase (NOS) activity as well as synthesis of AVP and oxytocin in the paraventricular (PVN) and supraoptic nuclei (SON), it is not known whether NOS activity in the hypothalamus changes in the diabetic patients who have plasma hyperosmolality with hyperglycaemia caused by insulin deficiency. |
| 218 | 9662044 | Expression of the neuronal (n) NOS gene in the PVN and SON in streptozotocin (STZ)-induced diabetic rats was investigated by using in situ hybridization histochemistry and NADPH-diaphorase histochemical staining. |
| 219 | 9662044 | The expression of nNOS gene and NADPH-diaphorase staining in the PVN and SON remarkably increased in STZ-induced diabetic rats compared to control rats. |
| 220 | 9662044 | Three weeks after administration of STZ, the diabetic rats were subcutaneously treated with insulin for 1 week, which resulted in significant suppression of the induction of nNOS, AVP and oxytocin gene expression in the PVN and SON. |
| 221 | 9662044 | Furthermore, the induction of nNOS gene expression in the PVN and SON was suppressed in STZ-induced diabetic rats treated with phlorizin and diet to normalize hyperglycaemia without insulin treatment. |
| 222 | 9662044 | These results suggest that upregulation of nNOS gene expression as well as AVP and oxytocin gene expression in the PVN and SON in STZ-induced diabetic rats may be associated with hyperglycaemia and plamsa hyperosmolality. |
| 223 | 9662044 | Plasma arginine vasopressin (AVP) is known to be elevated in patients with uncontrolled insulin-dependent diabetes mellitus who have plasma hyperosmolality with hyperglycaemia. |
| 224 | 9662044 | Although osmotic stimuli cause an increase in nitric oxide synthase (NOS) activity as well as synthesis of AVP and oxytocin in the paraventricular (PVN) and supraoptic nuclei (SON), it is not known whether NOS activity in the hypothalamus changes in the diabetic patients who have plasma hyperosmolality with hyperglycaemia caused by insulin deficiency. |
| 225 | 9662044 | Expression of the neuronal (n) NOS gene in the PVN and SON in streptozotocin (STZ)-induced diabetic rats was investigated by using in situ hybridization histochemistry and NADPH-diaphorase histochemical staining. |
| 226 | 9662044 | The expression of nNOS gene and NADPH-diaphorase staining in the PVN and SON remarkably increased in STZ-induced diabetic rats compared to control rats. |
| 227 | 9662044 | Three weeks after administration of STZ, the diabetic rats were subcutaneously treated with insulin for 1 week, which resulted in significant suppression of the induction of nNOS, AVP and oxytocin gene expression in the PVN and SON. |
| 228 | 9662044 | Furthermore, the induction of nNOS gene expression in the PVN and SON was suppressed in STZ-induced diabetic rats treated with phlorizin and diet to normalize hyperglycaemia without insulin treatment. |
| 229 | 9662044 | These results suggest that upregulation of nNOS gene expression as well as AVP and oxytocin gene expression in the PVN and SON in STZ-induced diabetic rats may be associated with hyperglycaemia and plamsa hyperosmolality. |
| 230 | 9662044 | Plasma arginine vasopressin (AVP) is known to be elevated in patients with uncontrolled insulin-dependent diabetes mellitus who have plasma hyperosmolality with hyperglycaemia. |
| 231 | 9662044 | Although osmotic stimuli cause an increase in nitric oxide synthase (NOS) activity as well as synthesis of AVP and oxytocin in the paraventricular (PVN) and supraoptic nuclei (SON), it is not known whether NOS activity in the hypothalamus changes in the diabetic patients who have plasma hyperosmolality with hyperglycaemia caused by insulin deficiency. |
| 232 | 9662044 | Expression of the neuronal (n) NOS gene in the PVN and SON in streptozotocin (STZ)-induced diabetic rats was investigated by using in situ hybridization histochemistry and NADPH-diaphorase histochemical staining. |
| 233 | 9662044 | The expression of nNOS gene and NADPH-diaphorase staining in the PVN and SON remarkably increased in STZ-induced diabetic rats compared to control rats. |
| 234 | 9662044 | Three weeks after administration of STZ, the diabetic rats were subcutaneously treated with insulin for 1 week, which resulted in significant suppression of the induction of nNOS, AVP and oxytocin gene expression in the PVN and SON. |
| 235 | 9662044 | Furthermore, the induction of nNOS gene expression in the PVN and SON was suppressed in STZ-induced diabetic rats treated with phlorizin and diet to normalize hyperglycaemia without insulin treatment. |
| 236 | 9662044 | These results suggest that upregulation of nNOS gene expression as well as AVP and oxytocin gene expression in the PVN and SON in STZ-induced diabetic rats may be associated with hyperglycaemia and plamsa hyperosmolality. |
| 237 | 9769333 | Central nervous system nitric oxide synthase activity regulates insulin secretion and insulin action. |
| 238 | 9769333 | Systemic inhibition of nitric oxide synthase (NOS) with NG-monomethyl-L-arginine (L-NMMA) causes acute insulin resistance (IR), but the mechanism is unknown. |
| 239 | 9769333 | The data suggest the novel concept that central NOS-dependent pathways may control peripheral insulin action and secretion. |
| 240 | 9769333 | Central nervous system nitric oxide synthase activity regulates insulin secretion and insulin action. |
| 241 | 9769333 | Systemic inhibition of nitric oxide synthase (NOS) with NG-monomethyl-L-arginine (L-NMMA) causes acute insulin resistance (IR), but the mechanism is unknown. |
| 242 | 9769333 | The data suggest the novel concept that central NOS-dependent pathways may control peripheral insulin action and secretion. |
| 243 | 9781316 | Inhibition of NOS activity blunts contraction-stimulated glucose transport but has no effect on insulin-stimulated glucose transport. |
| 244 | 9781316 | NOS protein expression is enhanced by chronic exercise suggesting that NO may play a role in the improved glucose tolerance and increased insulin sensitivity characteristic of the trained state. |
| 245 | 9781316 | Inhibition of NOS activity blunts contraction-stimulated glucose transport but has no effect on insulin-stimulated glucose transport. |
| 246 | 9781316 | NOS protein expression is enhanced by chronic exercise suggesting that NO may play a role in the improved glucose tolerance and increased insulin sensitivity characteristic of the trained state. |
| 247 | 9801272 | Increased prostaglandin E generation and enhanced nitric oxide synthase activity in the non-insulin-dependent diabetic embryo during organogenesis. |
| 248 | 9801272 | Embryonic development, prostaglandin E (PGE) generation and nitric oxide synthase (NOS) activity during organogenesis were evaluated in an experimental rat model of non-insulin-dependent diabetes (NIDD) generated by neonatal administration of streptozotocin. |
| 249 | 9858648 | This review discusses the role of (6R)-5,6,7,8-tetrahydrobiopterin (H4 biopterin) in the function of nitric oxide synthase (NOS), and the protective effect of H4 biopterin against nitric oxide (NO)- and/or reactive oxygen species-induced cytotoxicity. |
| 250 | 9867208 | This study examined the effects of short (1 and 3 weeks) and long term (32 weeks) diabetes on nNOS-containing neurons of the retina using NADPH diaphorase (NADPHd) histochemistry. |
| 251 | 9881841 | It is my hypothesis that a breakdown in the urea cycle (via activation of nitric oxide synthase (NOS)), a primary metabolic pathway, whereby nitric oxide production is competitively favored over urea production, is responsible for generating the major source of pathogenic nitric oxide resulting in the death of the beta cells of the pancreas. |
| 252 | 10077349 | The increased ovarian proteolytic activity associated with ovulation is controlled by locally produced specific inhibitors, plasminogen activator inhibitor-1 (PAI-1) and tissue inhibitor of metalloproteases-1 (TIMP-1). |
| 253 | 10077349 | These include steroids, vascular endothelial growth factor (VEGF), cytokines, eicosanoids, platelet activating factor (PAF), nitric oxide and nitric oxide synthase (NO/NOS), kinins and oxygen radicals. |
| 254 | 10097254 | The animals were divided into three groups and treated for 4 weeks with daily subcutaneous injections of insulin (25U/kg body weight) with or without oral administration of l-nitro-arginine methyl ester (L-NAME, 50mg/kg/day body weight as drinking water), an inhibitor of NO synthase (NOS). |
| 255 | 10097254 | Insulin treatment resulted in a decrease in plasma glucose and blood pressure, and an increase in both NO metabolites (NOx) in the plasma and NOS activity in the aorta tissue. |
| 256 | 10097254 | L-NAME treatment blunted not only the antihypertensive effect of insulin but also the changes in NOx and NOS activity. |
| 257 | 10097254 | These findings suggest that insulin reduces blood pressure in the ZDF rat by stimulating NOS activation and NO production. |
| 258 | 10097254 | The animals were divided into three groups and treated for 4 weeks with daily subcutaneous injections of insulin (25U/kg body weight) with or without oral administration of l-nitro-arginine methyl ester (L-NAME, 50mg/kg/day body weight as drinking water), an inhibitor of NO synthase (NOS). |
| 259 | 10097254 | Insulin treatment resulted in a decrease in plasma glucose and blood pressure, and an increase in both NO metabolites (NOx) in the plasma and NOS activity in the aorta tissue. |
| 260 | 10097254 | L-NAME treatment blunted not only the antihypertensive effect of insulin but also the changes in NOx and NOS activity. |
| 261 | 10097254 | These findings suggest that insulin reduces blood pressure in the ZDF rat by stimulating NOS activation and NO production. |
| 262 | 10097254 | The animals were divided into three groups and treated for 4 weeks with daily subcutaneous injections of insulin (25U/kg body weight) with or without oral administration of l-nitro-arginine methyl ester (L-NAME, 50mg/kg/day body weight as drinking water), an inhibitor of NO synthase (NOS). |
| 263 | 10097254 | Insulin treatment resulted in a decrease in plasma glucose and blood pressure, and an increase in both NO metabolites (NOx) in the plasma and NOS activity in the aorta tissue. |
| 264 | 10097254 | L-NAME treatment blunted not only the antihypertensive effect of insulin but also the changes in NOx and NOS activity. |
| 265 | 10097254 | These findings suggest that insulin reduces blood pressure in the ZDF rat by stimulating NOS activation and NO production. |
| 266 | 10097254 | The animals were divided into three groups and treated for 4 weeks with daily subcutaneous injections of insulin (25U/kg body weight) with or without oral administration of l-nitro-arginine methyl ester (L-NAME, 50mg/kg/day body weight as drinking water), an inhibitor of NO synthase (NOS). |
| 267 | 10097254 | Insulin treatment resulted in a decrease in plasma glucose and blood pressure, and an increase in both NO metabolites (NOx) in the plasma and NOS activity in the aorta tissue. |
| 268 | 10097254 | L-NAME treatment blunted not only the antihypertensive effect of insulin but also the changes in NOx and NOS activity. |
| 269 | 10097254 | These findings suggest that insulin reduces blood pressure in the ZDF rat by stimulating NOS activation and NO production. |
| 270 | 10323305 | Nitric oxide synthase (NOS) activity was assessed by the conversion of 3H-L-arginine to 3H-L-citrulline in homogenates of anococcygeus muscles obtained from 8-week diabetic rats and control rats. |
| 271 | 10323305 | NOS-immunoreactive and NADPH-diaphorase reactive nerve terminals were found to be sparsely distributed throughout longitudinal sections or whole mounts of anococcygeus muscles from both control and diabetic rats. |
| 272 | 10323305 | Nitric oxide synthase (NOS) activity was assessed by the conversion of 3H-L-arginine to 3H-L-citrulline in homogenates of anococcygeus muscles obtained from 8-week diabetic rats and control rats. |
| 273 | 10323305 | NOS-immunoreactive and NADPH-diaphorase reactive nerve terminals were found to be sparsely distributed throughout longitudinal sections or whole mounts of anococcygeus muscles from both control and diabetic rats. |
| 274 | 10337852 | The aim of the present study was to evaluate the action of plasma from insulin-dependent diabetic (IDDM) pregnant women on nitric oxide synthase (NOS) activity in cultured human umbilical vein endothelial cells (HUVECs). |
| 275 | 10337852 | We observed a significant increase in NOS activity, intracellular calcium, and Na+/K+-ATPase activity in cultured HUVECs exposed to IDDM plasma. |
| 276 | 10337852 | The aim of the present study was to evaluate the action of plasma from insulin-dependent diabetic (IDDM) pregnant women on nitric oxide synthase (NOS) activity in cultured human umbilical vein endothelial cells (HUVECs). |
| 277 | 10337852 | We observed a significant increase in NOS activity, intracellular calcium, and Na+/K+-ATPase activity in cultured HUVECs exposed to IDDM plasma. |
| 278 | 10338373 | We have investigated the expression and localization of endothelium-derived nitric oxide synthase (eNOS) and the effect of eNOS on placental human chorionic gonadotrophin (HCG) release. eNOS mRNA was found to be expressed in all tissues, with its expression significantly (P<0.05) increased across gestation. |
| 279 | 10338373 | HCG was found to colocalize with eNOS in trophoblasts, but not in endothelia. |
| 280 | 10338373 | When placental explants were perifused, exposure to the NOS substrate, the NO donor, I-arginine and trinitroglycerol evoked a prompt, albeit transient, increase of HCG release. |
| 281 | 10338373 | The NOS inhibitor delayed, but did not block arginine-induced HCG release. |
| 282 | 10338373 | A role for NO in the acute endocrine modulation of the placenta is suggested by the colocalization of eNOS with HCG in human trophoblasts and the prompt secretion of HCG in response to agents which increase NO concentrations. |
| 283 | 10338373 | We have investigated the expression and localization of endothelium-derived nitric oxide synthase (eNOS) and the effect of eNOS on placental human chorionic gonadotrophin (HCG) release. eNOS mRNA was found to be expressed in all tissues, with its expression significantly (P<0.05) increased across gestation. |
| 284 | 10338373 | HCG was found to colocalize with eNOS in trophoblasts, but not in endothelia. |
| 285 | 10338373 | When placental explants were perifused, exposure to the NOS substrate, the NO donor, I-arginine and trinitroglycerol evoked a prompt, albeit transient, increase of HCG release. |
| 286 | 10338373 | The NOS inhibitor delayed, but did not block arginine-induced HCG release. |
| 287 | 10338373 | A role for NO in the acute endocrine modulation of the placenta is suggested by the colocalization of eNOS with HCG in human trophoblasts and the prompt secretion of HCG in response to agents which increase NO concentrations. |
| 288 | 10369805 | Endothelial nitric oxide synthase (NOS) protein and mRNA have been identified and calcium-dependent NOS activity has been measured in human placentae during normal pregnancy. |
| 289 | 10377817 | STZ-induced diabetic rats showed decreases in nociceptive threshold and NADPH-diaphorase positive neurons, nNOS level and cGMP content of DRG at 12 weeks after induction of diabetes. |
| 290 | 10398211 | We evaluated the effects of angiotensin II and an angiotensin-converting enzyme inhibitor (cilazapril) on nerve blood flow (NBF) and electrophysiology in control and diabetic rats. |
| 291 | 10398211 | We topically applied the nitric oxide synthase (NOS) inhibitor, NG-nitro-L-arginine, on sciatic nerve and observed reduced inhibition of NBF in EDN, which was correctable with a cilazapril diet. |
| 292 | 10398211 | These results suggest that diabetic neuropathy may have an increasing vasopressor action with angiotensin II and this is likely to be the mechanism of NOS inhibition. |
| 293 | 10398211 | We evaluated the effects of angiotensin II and an angiotensin-converting enzyme inhibitor (cilazapril) on nerve blood flow (NBF) and electrophysiology in control and diabetic rats. |
| 294 | 10398211 | We topically applied the nitric oxide synthase (NOS) inhibitor, NG-nitro-L-arginine, on sciatic nerve and observed reduced inhibition of NBF in EDN, which was correctable with a cilazapril diet. |
| 295 | 10398211 | These results suggest that diabetic neuropathy may have an increasing vasopressor action with angiotensin II and this is likely to be the mechanism of NOS inhibition. |
| 296 | 10404280 | NADPH diaphorase staining was used to identify NOS and immunostaining technique was used to identify nNOS in the penile nerve fibers. |
| 297 | 10404280 | RT-PCR was used to identify mRNA expression of nNOS, eNOS, iNOS, ER-beta, ER-alpha, NGF, IGF-I, TGF-beta 1, and AR. |
| 298 | 10404280 | Western blot was used to identify nNOS, IGF-I, NGF, and TFG-beta protein expressions. |
| 299 | 10404280 | RT-PCR showed down-regulation of nNOS (large form), iNOS and ER-beta mRNA expression, Immunoblot showed down-regulation of nNOS protein expression and nNOS immunostaining showed less positive staining in the dorsal and intracavernous nerves in the diabetic group. |
| 300 | 10404280 | NADPH diaphorase staining was used to identify NOS and immunostaining technique was used to identify nNOS in the penile nerve fibers. |
| 301 | 10404280 | RT-PCR was used to identify mRNA expression of nNOS, eNOS, iNOS, ER-beta, ER-alpha, NGF, IGF-I, TGF-beta 1, and AR. |
| 302 | 10404280 | Western blot was used to identify nNOS, IGF-I, NGF, and TFG-beta protein expressions. |
| 303 | 10404280 | RT-PCR showed down-regulation of nNOS (large form), iNOS and ER-beta mRNA expression, Immunoblot showed down-regulation of nNOS protein expression and nNOS immunostaining showed less positive staining in the dorsal and intracavernous nerves in the diabetic group. |
| 304 | 10404280 | NADPH diaphorase staining was used to identify NOS and immunostaining technique was used to identify nNOS in the penile nerve fibers. |
| 305 | 10404280 | RT-PCR was used to identify mRNA expression of nNOS, eNOS, iNOS, ER-beta, ER-alpha, NGF, IGF-I, TGF-beta 1, and AR. |
| 306 | 10404280 | Western blot was used to identify nNOS, IGF-I, NGF, and TFG-beta protein expressions. |
| 307 | 10404280 | RT-PCR showed down-regulation of nNOS (large form), iNOS and ER-beta mRNA expression, Immunoblot showed down-regulation of nNOS protein expression and nNOS immunostaining showed less positive staining in the dorsal and intracavernous nerves in the diabetic group. |
| 308 | 10404280 | NADPH diaphorase staining was used to identify NOS and immunostaining technique was used to identify nNOS in the penile nerve fibers. |
| 309 | 10404280 | RT-PCR was used to identify mRNA expression of nNOS, eNOS, iNOS, ER-beta, ER-alpha, NGF, IGF-I, TGF-beta 1, and AR. |
| 310 | 10404280 | Western blot was used to identify nNOS, IGF-I, NGF, and TFG-beta protein expressions. |
| 311 | 10404280 | RT-PCR showed down-regulation of nNOS (large form), iNOS and ER-beta mRNA expression, Immunoblot showed down-regulation of nNOS protein expression and nNOS immunostaining showed less positive staining in the dorsal and intracavernous nerves in the diabetic group. |
| 312 | 10444370 | In contrast, insulin-stimulated 2-deoxyglucose transport was enhanced (P < 0.03) by chronic NOS inhibition (5.29 +/- 0.83 nmol/g/min) compared to control rats (2.21 +/- 0.90 nmol/g/min). |
| 313 | 10507551 | In an attempt to know the role of nitric oxide in the disease of insulin-dependent diabetic mellitus (IDDM), the present study examined the change of nitric oxide synthase (NOS) both the activity and gene expression in cerebrocortex of streptozotocin-induced diabetic rats (STZ-diabetic rats). |
| 314 | 10523028 | In the present work we studied in vitro the action of low density lipoproteins (LDL) isolated from normolipemic insulin-dependent diabetic (IDDM) patients on transmembrane cation transport, nitric oxide synthase (NOS) activity, and aggregating response to stimuli of platelets from healthy subjects to elucidate whether the modified interaction between circulating lipoproteins and cells might be one of the pathogenetic mechanisms of the increased platelet activation in IDDM. |
| 315 | 10523028 | Platelet aggregation responses to ADP, NOS activity, cytosolic Ca2+ concentrations, and platelet membrane Na+/K+-adenosine triphosphatase (Na+/K+-ATPase) and Ca2+-ATPase activities were measured after incubation. |
| 316 | 10523028 | IDDM LDL significantly increased the platelet aggregating response to ADP, cytosolic Ca2+ concentrations, and plasma membrane Ca2+-ATPase activity and significantly reduced NOS activity and platelet membrane Na+/K+-ATPase activity compared with those of platelets incubated in buffer or cells incubated with control LDL. |
| 317 | 10523028 | Both the decreased activity of NOS and the higher cytoplasmic concentrations of Ca2+ might cause increased platelet activation, as observed in IDDM. |
| 318 | 10523028 | In the present work we studied in vitro the action of low density lipoproteins (LDL) isolated from normolipemic insulin-dependent diabetic (IDDM) patients on transmembrane cation transport, nitric oxide synthase (NOS) activity, and aggregating response to stimuli of platelets from healthy subjects to elucidate whether the modified interaction between circulating lipoproteins and cells might be one of the pathogenetic mechanisms of the increased platelet activation in IDDM. |
| 319 | 10523028 | Platelet aggregation responses to ADP, NOS activity, cytosolic Ca2+ concentrations, and platelet membrane Na+/K+-adenosine triphosphatase (Na+/K+-ATPase) and Ca2+-ATPase activities were measured after incubation. |
| 320 | 10523028 | IDDM LDL significantly increased the platelet aggregating response to ADP, cytosolic Ca2+ concentrations, and plasma membrane Ca2+-ATPase activity and significantly reduced NOS activity and platelet membrane Na+/K+-ATPase activity compared with those of platelets incubated in buffer or cells incubated with control LDL. |
| 321 | 10523028 | Both the decreased activity of NOS and the higher cytoplasmic concentrations of Ca2+ might cause increased platelet activation, as observed in IDDM. |
| 322 | 10523028 | In the present work we studied in vitro the action of low density lipoproteins (LDL) isolated from normolipemic insulin-dependent diabetic (IDDM) patients on transmembrane cation transport, nitric oxide synthase (NOS) activity, and aggregating response to stimuli of platelets from healthy subjects to elucidate whether the modified interaction between circulating lipoproteins and cells might be one of the pathogenetic mechanisms of the increased platelet activation in IDDM. |
| 323 | 10523028 | Platelet aggregation responses to ADP, NOS activity, cytosolic Ca2+ concentrations, and platelet membrane Na+/K+-adenosine triphosphatase (Na+/K+-ATPase) and Ca2+-ATPase activities were measured after incubation. |
| 324 | 10523028 | IDDM LDL significantly increased the platelet aggregating response to ADP, cytosolic Ca2+ concentrations, and plasma membrane Ca2+-ATPase activity and significantly reduced NOS activity and platelet membrane Na+/K+-ATPase activity compared with those of platelets incubated in buffer or cells incubated with control LDL. |
| 325 | 10523028 | Both the decreased activity of NOS and the higher cytoplasmic concentrations of Ca2+ might cause increased platelet activation, as observed in IDDM. |
| 326 | 10523028 | In the present work we studied in vitro the action of low density lipoproteins (LDL) isolated from normolipemic insulin-dependent diabetic (IDDM) patients on transmembrane cation transport, nitric oxide synthase (NOS) activity, and aggregating response to stimuli of platelets from healthy subjects to elucidate whether the modified interaction between circulating lipoproteins and cells might be one of the pathogenetic mechanisms of the increased platelet activation in IDDM. |
| 327 | 10523028 | Platelet aggregation responses to ADP, NOS activity, cytosolic Ca2+ concentrations, and platelet membrane Na+/K+-adenosine triphosphatase (Na+/K+-ATPase) and Ca2+-ATPase activities were measured after incubation. |
| 328 | 10523028 | IDDM LDL significantly increased the platelet aggregating response to ADP, cytosolic Ca2+ concentrations, and plasma membrane Ca2+-ATPase activity and significantly reduced NOS activity and platelet membrane Na+/K+-ATPase activity compared with those of platelets incubated in buffer or cells incubated with control LDL. |
| 329 | 10523028 | Both the decreased activity of NOS and the higher cytoplasmic concentrations of Ca2+ might cause increased platelet activation, as observed in IDDM. |
| 330 | 10637124 | The addition of nitric oxide synthase (NOS) inhibitors (1 mM N(G)-nitro-l-arginine methyl ester, 600 microM N(G)-monomethyl-l-arginine) in the incubating medium reduces and NO donors (SIN-1, 300 microM spermine suppress, NONOate 100 microM) increases ET levels in pancreatic slices from C and D animals. |
| 331 | 10637124 | When tissues are incubated in the presence of endothelin 1 (ET-1) (10(-7) M), NOS activity is higher in C pancreas, while the ET-receptor antagonist bosentan (B) decreases NOS levels in D but not in C tissues. |
| 332 | 10637124 | When pancreatic arachidonic acid (AA) conversion to prostaglandins was explored, ET-1 increased PGF(2alpha), PGE(2), and TXB(2) levels in C but not in D tissues. |
| 333 | 10637124 | The addition of nitric oxide synthase (NOS) inhibitors (1 mM N(G)-nitro-l-arginine methyl ester, 600 microM N(G)-monomethyl-l-arginine) in the incubating medium reduces and NO donors (SIN-1, 300 microM spermine suppress, NONOate 100 microM) increases ET levels in pancreatic slices from C and D animals. |
| 334 | 10637124 | When tissues are incubated in the presence of endothelin 1 (ET-1) (10(-7) M), NOS activity is higher in C pancreas, while the ET-receptor antagonist bosentan (B) decreases NOS levels in D but not in C tissues. |
| 335 | 10637124 | When pancreatic arachidonic acid (AA) conversion to prostaglandins was explored, ET-1 increased PGF(2alpha), PGE(2), and TXB(2) levels in C but not in D tissues. |
| 336 | 10679477 | The aim of this study was to further define the role of NO in the control of myocardial glucose metabolism and the nitric oxide synthase (NOS) isoform responsible using transgenic animals lacking endothelial NOS (ecNOS). |
| 337 | 10679490 | Regulation of endothelial nitric oxide synthase expression by albumin-derived advanced glycosylation end products. |
| 338 | 10679490 | We examined whether albumin-derived advanced glycosylation end products (AGEs) downregulate the expression of endothelial nitric oxide synthase (NOS). |
| 339 | 10679490 | Significant reductions in NOS activity and cGMP levels in bovine aortic endothelial cells were observed when exposed to different concentrations of albumin-derived AGEs. |
| 340 | 10679490 | Regulation of endothelial nitric oxide synthase expression by albumin-derived advanced glycosylation end products. |
| 341 | 10679490 | We examined whether albumin-derived advanced glycosylation end products (AGEs) downregulate the expression of endothelial nitric oxide synthase (NOS). |
| 342 | 10679490 | Significant reductions in NOS activity and cGMP levels in bovine aortic endothelial cells were observed when exposed to different concentrations of albumin-derived AGEs. |
| 343 | 10679513 | The interaction of this pathway and the renin-angiotensin system was studied in separate groups of rats pretreated with the angiotensin II receptor blocker losartan; these rats were compared with rats treated with losartan alone. |
| 344 | 10679513 | Furthermore, renal responses in diabetic rats were attenuated by angiotensin II receptor blockade, whereas losartan alone induced hemodynamic changes that were opposite those seen with neuronal nitric oxide synthase inhibition. |
| 345 | 10690935 | Effect of insulin on human aortic endothelial nitric oxide synthase. |
| 346 | 10690935 | In view of these observations and the fact that insulin-induced vasodilation is impaired in insulin-resistant states like type 2 diabetes and obesity, we have investigated the hypothesis that insulin may induce the expression of endothelial nitric oxide synthase (e-NOS) in endothelial cells grown from human aortae (HAECs), human lower-limb veins, and human umbilical veins (HUVECs), and microvascular endothelial cells (MVECs) from human adipose tissue. |
| 347 | 10690935 | There was no detectable level of the inducible NOS isoform (i-NOS), and this effect of insulin was independent of cell proliferation. |
| 348 | 10732689 | The enhanced NADPH-diaphorase staining may be due to a deficiency of NOS substrate L-arginine in the endothelium and nerves of diabetic tissues. |
| 349 | 10735554 | Nitric oxide synthase (NOS) activity is enhanced in proestrous ovaries from type I diabetic rats, but cGMP levels are diminished. |
| 350 | 10810880 | Incubation of human aortic endothelial cells(HAEC) with glycated LDL had little influence on the expression of antioxidant enzymes such as nitric oxide synthase(NOS), Cu2+Zn(2+)-superoxide dismutase (Cu2+Zn(2+)-SOD), catalase, and p22 phox in the cells. |
| 351 | 10810880 | In contrast, exposure of glycated HDL induced a marked decrease of Cu2+Zn(2+)-SOD, catalase, and endothelial NOS as well as a slight increase of p22 phox in HAEC in term of both protein and mRNA expression, suggesting that increased formation of reactive oxygen species such as O2- and OH radical participate in the deterioration for the function of vascular endothelial cells in diabetic patients. |
| 352 | 10810880 | Incubation of human aortic endothelial cells(HAEC) with glycated LDL had little influence on the expression of antioxidant enzymes such as nitric oxide synthase(NOS), Cu2+Zn(2+)-superoxide dismutase (Cu2+Zn(2+)-SOD), catalase, and p22 phox in the cells. |
| 353 | 10810880 | In contrast, exposure of glycated HDL induced a marked decrease of Cu2+Zn(2+)-SOD, catalase, and endothelial NOS as well as a slight increase of p22 phox in HAEC in term of both protein and mRNA expression, suggesting that increased formation of reactive oxygen species such as O2- and OH radical participate in the deterioration for the function of vascular endothelial cells in diabetic patients. |
| 354 | 10835293 | The involvement of NO in nickel-induced hyperglycemia was evident by the observation that pretreatment of rats with NG-monomethyl-l-arginine (10 to 50 micromol/kg; ip), an inhibitor of nitric oxide synthase (NOS), significantly attenuated the nickel-mediated increase in the plasma glucose levels in a dose-dependent fashion. |
| 355 | 10902810 | Insulin inhibits the expression of intercellular adhesion molecule-1 by human aortic endothelial cells through stimulation of nitric oxide. |
| 356 | 10902810 | As it has been suggested that insulin and hyperinsulinemia may have a role in atherogenesis, we have now investigated whether insulin has an effect on the expression of ICAM-1 on human aortic endothelial cells (HAEC). |
| 357 | 10902810 | Insulin (100 and 1000 microU/mL) caused a decrease in the expression of ICAM-1 (messenger ribonucleic acid and protein) by these cells in a dose-dependent manner after incubation for 2 days. |
| 358 | 10902810 | This decrease was associated with a concomitant increase in endothelial nitric oxide synthase (NOS) expression also induced by insulin. |
| 359 | 10902810 | To examine whether the insulin-induced inhibition of ICAM-1 was mediated by nitric oxide (NO) from increased endothelial NOS, HAEC were treated with N(omega)-nitro-L-arginine, a NOS inhibitor. |
| 360 | 10902810 | N(omega)-Nitro-L-arginine inhibited the insulin-induced decrease in ICAM-1 expression in HAEC at the messenger ribonucleic acid and protein levels. |
| 361 | 10902810 | Thus, the inhibitory effect of insulin on ICAM-1 expression is mediated by NO. |
| 362 | 10902810 | We conclude that insulin reduces the expression of the proinflammatory adhesion molecule ICAM-1 through an increase in the expression of NOS and NO generation and that insulin may have a potential antiinflammatory and antiatherosclerotic effect rather than a proatherosclerotic effect. |
| 363 | 10902810 | Insulin inhibits the expression of intercellular adhesion molecule-1 by human aortic endothelial cells through stimulation of nitric oxide. |
| 364 | 10902810 | As it has been suggested that insulin and hyperinsulinemia may have a role in atherogenesis, we have now investigated whether insulin has an effect on the expression of ICAM-1 on human aortic endothelial cells (HAEC). |
| 365 | 10902810 | Insulin (100 and 1000 microU/mL) caused a decrease in the expression of ICAM-1 (messenger ribonucleic acid and protein) by these cells in a dose-dependent manner after incubation for 2 days. |
| 366 | 10902810 | This decrease was associated with a concomitant increase in endothelial nitric oxide synthase (NOS) expression also induced by insulin. |
| 367 | 10902810 | To examine whether the insulin-induced inhibition of ICAM-1 was mediated by nitric oxide (NO) from increased endothelial NOS, HAEC were treated with N(omega)-nitro-L-arginine, a NOS inhibitor. |
| 368 | 10902810 | N(omega)-Nitro-L-arginine inhibited the insulin-induced decrease in ICAM-1 expression in HAEC at the messenger ribonucleic acid and protein levels. |
| 369 | 10902810 | Thus, the inhibitory effect of insulin on ICAM-1 expression is mediated by NO. |
| 370 | 10902810 | We conclude that insulin reduces the expression of the proinflammatory adhesion molecule ICAM-1 through an increase in the expression of NOS and NO generation and that insulin may have a potential antiinflammatory and antiatherosclerotic effect rather than a proatherosclerotic effect. |
| 371 | 10902810 | Insulin inhibits the expression of intercellular adhesion molecule-1 by human aortic endothelial cells through stimulation of nitric oxide. |
| 372 | 10902810 | As it has been suggested that insulin and hyperinsulinemia may have a role in atherogenesis, we have now investigated whether insulin has an effect on the expression of ICAM-1 on human aortic endothelial cells (HAEC). |
| 373 | 10902810 | Insulin (100 and 1000 microU/mL) caused a decrease in the expression of ICAM-1 (messenger ribonucleic acid and protein) by these cells in a dose-dependent manner after incubation for 2 days. |
| 374 | 10902810 | This decrease was associated with a concomitant increase in endothelial nitric oxide synthase (NOS) expression also induced by insulin. |
| 375 | 10902810 | To examine whether the insulin-induced inhibition of ICAM-1 was mediated by nitric oxide (NO) from increased endothelial NOS, HAEC were treated with N(omega)-nitro-L-arginine, a NOS inhibitor. |
| 376 | 10902810 | N(omega)-Nitro-L-arginine inhibited the insulin-induced decrease in ICAM-1 expression in HAEC at the messenger ribonucleic acid and protein levels. |
| 377 | 10902810 | Thus, the inhibitory effect of insulin on ICAM-1 expression is mediated by NO. |
| 378 | 10902810 | We conclude that insulin reduces the expression of the proinflammatory adhesion molecule ICAM-1 through an increase in the expression of NOS and NO generation and that insulin may have a potential antiinflammatory and antiatherosclerotic effect rather than a proatherosclerotic effect. |
| 379 | 10905473 | Mice with gene disruption of both endothelial and neuronal nitric oxide synthase exhibit insulin resistance. |
| 380 | 10905473 | Studies from our laboratory using acute pharmacologic blockade of nitric oxide synthase (NOS) activity have suggested that nitric oxide (NO) has an important role in regulating carbohydrate metabolism. |
| 381 | 10905473 | We now report on insulin sensitivity in mice with targeted disruptions in endothelial NOS (eNOS) and neuronal NOS (nNOS) genes compared with their wild-type (WT) counterparts. |
| 382 | 10905473 | GIR was significantly reduced (37%, P = 0.001) in the eNOS knockout (KO) mice compared with the WT mice, with values for the nNOS mice being intermediate. |
| 383 | 10905473 | EGO was completely suppressed in the nNOS and WT mice during insulin infusion, but not in the eNOS mice. |
| 384 | 10905473 | Even so, the eNOS mice displayed significantly reduced whole-body GDRs compared with those of the WT mice (82.67+/-10.77 vs. 103.67+/-3.47 mg x kg(-1) x min(-1), P = 0.03). eNOS KO mice are insulin resistant at the level of the liver and peripheral tissues, whereas the nNOS KO mice are insulin resistant only in the latter. |
| 385 | 10905473 | These data indicate that NO plays a role in modulating insulin sensitivity and carbohydrate metabolism and that the eNOS isoform may play a dominant role relative to nNOS. |
| 386 | 10905473 | Mice with gene disruption of both endothelial and neuronal nitric oxide synthase exhibit insulin resistance. |
| 387 | 10905473 | Studies from our laboratory using acute pharmacologic blockade of nitric oxide synthase (NOS) activity have suggested that nitric oxide (NO) has an important role in regulating carbohydrate metabolism. |
| 388 | 10905473 | We now report on insulin sensitivity in mice with targeted disruptions in endothelial NOS (eNOS) and neuronal NOS (nNOS) genes compared with their wild-type (WT) counterparts. |
| 389 | 10905473 | GIR was significantly reduced (37%, P = 0.001) in the eNOS knockout (KO) mice compared with the WT mice, with values for the nNOS mice being intermediate. |
| 390 | 10905473 | EGO was completely suppressed in the nNOS and WT mice during insulin infusion, but not in the eNOS mice. |
| 391 | 10905473 | Even so, the eNOS mice displayed significantly reduced whole-body GDRs compared with those of the WT mice (82.67+/-10.77 vs. 103.67+/-3.47 mg x kg(-1) x min(-1), P = 0.03). eNOS KO mice are insulin resistant at the level of the liver and peripheral tissues, whereas the nNOS KO mice are insulin resistant only in the latter. |
| 392 | 10905473 | These data indicate that NO plays a role in modulating insulin sensitivity and carbohydrate metabolism and that the eNOS isoform may play a dominant role relative to nNOS. |
| 393 | 10905473 | Mice with gene disruption of both endothelial and neuronal nitric oxide synthase exhibit insulin resistance. |
| 394 | 10905473 | Studies from our laboratory using acute pharmacologic blockade of nitric oxide synthase (NOS) activity have suggested that nitric oxide (NO) has an important role in regulating carbohydrate metabolism. |
| 395 | 10905473 | We now report on insulin sensitivity in mice with targeted disruptions in endothelial NOS (eNOS) and neuronal NOS (nNOS) genes compared with their wild-type (WT) counterparts. |
| 396 | 10905473 | GIR was significantly reduced (37%, P = 0.001) in the eNOS knockout (KO) mice compared with the WT mice, with values for the nNOS mice being intermediate. |
| 397 | 10905473 | EGO was completely suppressed in the nNOS and WT mice during insulin infusion, but not in the eNOS mice. |
| 398 | 10905473 | Even so, the eNOS mice displayed significantly reduced whole-body GDRs compared with those of the WT mice (82.67+/-10.77 vs. 103.67+/-3.47 mg x kg(-1) x min(-1), P = 0.03). eNOS KO mice are insulin resistant at the level of the liver and peripheral tissues, whereas the nNOS KO mice are insulin resistant only in the latter. |
| 399 | 10905473 | These data indicate that NO plays a role in modulating insulin sensitivity and carbohydrate metabolism and that the eNOS isoform may play a dominant role relative to nNOS. |
| 400 | 10905473 | Mice with gene disruption of both endothelial and neuronal nitric oxide synthase exhibit insulin resistance. |
| 401 | 10905473 | Studies from our laboratory using acute pharmacologic blockade of nitric oxide synthase (NOS) activity have suggested that nitric oxide (NO) has an important role in regulating carbohydrate metabolism. |
| 402 | 10905473 | We now report on insulin sensitivity in mice with targeted disruptions in endothelial NOS (eNOS) and neuronal NOS (nNOS) genes compared with their wild-type (WT) counterparts. |
| 403 | 10905473 | GIR was significantly reduced (37%, P = 0.001) in the eNOS knockout (KO) mice compared with the WT mice, with values for the nNOS mice being intermediate. |
| 404 | 10905473 | EGO was completely suppressed in the nNOS and WT mice during insulin infusion, but not in the eNOS mice. |
| 405 | 10905473 | Even so, the eNOS mice displayed significantly reduced whole-body GDRs compared with those of the WT mice (82.67+/-10.77 vs. 103.67+/-3.47 mg x kg(-1) x min(-1), P = 0.03). eNOS KO mice are insulin resistant at the level of the liver and peripheral tissues, whereas the nNOS KO mice are insulin resistant only in the latter. |
| 406 | 10905473 | These data indicate that NO plays a role in modulating insulin sensitivity and carbohydrate metabolism and that the eNOS isoform may play a dominant role relative to nNOS. |
| 407 | 10905473 | Mice with gene disruption of both endothelial and neuronal nitric oxide synthase exhibit insulin resistance. |
| 408 | 10905473 | Studies from our laboratory using acute pharmacologic blockade of nitric oxide synthase (NOS) activity have suggested that nitric oxide (NO) has an important role in regulating carbohydrate metabolism. |
| 409 | 10905473 | We now report on insulin sensitivity in mice with targeted disruptions in endothelial NOS (eNOS) and neuronal NOS (nNOS) genes compared with their wild-type (WT) counterparts. |
| 410 | 10905473 | GIR was significantly reduced (37%, P = 0.001) in the eNOS knockout (KO) mice compared with the WT mice, with values for the nNOS mice being intermediate. |
| 411 | 10905473 | EGO was completely suppressed in the nNOS and WT mice during insulin infusion, but not in the eNOS mice. |
| 412 | 10905473 | Even so, the eNOS mice displayed significantly reduced whole-body GDRs compared with those of the WT mice (82.67+/-10.77 vs. 103.67+/-3.47 mg x kg(-1) x min(-1), P = 0.03). eNOS KO mice are insulin resistant at the level of the liver and peripheral tissues, whereas the nNOS KO mice are insulin resistant only in the latter. |
| 413 | 10905473 | These data indicate that NO plays a role in modulating insulin sensitivity and carbohydrate metabolism and that the eNOS isoform may play a dominant role relative to nNOS. |
| 414 | 10905473 | Mice with gene disruption of both endothelial and neuronal nitric oxide synthase exhibit insulin resistance. |
| 415 | 10905473 | Studies from our laboratory using acute pharmacologic blockade of nitric oxide synthase (NOS) activity have suggested that nitric oxide (NO) has an important role in regulating carbohydrate metabolism. |
| 416 | 10905473 | We now report on insulin sensitivity in mice with targeted disruptions in endothelial NOS (eNOS) and neuronal NOS (nNOS) genes compared with their wild-type (WT) counterparts. |
| 417 | 10905473 | GIR was significantly reduced (37%, P = 0.001) in the eNOS knockout (KO) mice compared with the WT mice, with values for the nNOS mice being intermediate. |
| 418 | 10905473 | EGO was completely suppressed in the nNOS and WT mice during insulin infusion, but not in the eNOS mice. |
| 419 | 10905473 | Even so, the eNOS mice displayed significantly reduced whole-body GDRs compared with those of the WT mice (82.67+/-10.77 vs. 103.67+/-3.47 mg x kg(-1) x min(-1), P = 0.03). eNOS KO mice are insulin resistant at the level of the liver and peripheral tissues, whereas the nNOS KO mice are insulin resistant only in the latter. |
| 420 | 10905473 | These data indicate that NO plays a role in modulating insulin sensitivity and carbohydrate metabolism and that the eNOS isoform may play a dominant role relative to nNOS. |
| 421 | 10905473 | Mice with gene disruption of both endothelial and neuronal nitric oxide synthase exhibit insulin resistance. |
| 422 | 10905473 | Studies from our laboratory using acute pharmacologic blockade of nitric oxide synthase (NOS) activity have suggested that nitric oxide (NO) has an important role in regulating carbohydrate metabolism. |
| 423 | 10905473 | We now report on insulin sensitivity in mice with targeted disruptions in endothelial NOS (eNOS) and neuronal NOS (nNOS) genes compared with their wild-type (WT) counterparts. |
| 424 | 10905473 | GIR was significantly reduced (37%, P = 0.001) in the eNOS knockout (KO) mice compared with the WT mice, with values for the nNOS mice being intermediate. |
| 425 | 10905473 | EGO was completely suppressed in the nNOS and WT mice during insulin infusion, but not in the eNOS mice. |
| 426 | 10905473 | Even so, the eNOS mice displayed significantly reduced whole-body GDRs compared with those of the WT mice (82.67+/-10.77 vs. 103.67+/-3.47 mg x kg(-1) x min(-1), P = 0.03). eNOS KO mice are insulin resistant at the level of the liver and peripheral tissues, whereas the nNOS KO mice are insulin resistant only in the latter. |
| 427 | 10905473 | These data indicate that NO plays a role in modulating insulin sensitivity and carbohydrate metabolism and that the eNOS isoform may play a dominant role relative to nNOS. |
| 428 | 10925066 | Inhibition of renal nitric oxide synthase (NOS) resulted in a greater increase of TGF reactivity in diabetic rats than in control rats. |
| 429 | 10925066 | Diabetic rats also showed increased excretion rates of albumin and THP. |
| 430 | 10930440 | Insulin restores neuronal nitric oxide synthase expression and function that is lost in diabetic gastropathy. |
| 431 | 10930440 | The decline of nNOS in diabetic mice does not result from loss of myenteric neurons. nNOS expression and pyloric function are restored to normal levels by insulin treatment. |
| 432 | 10930440 | Thus diabetic gastropathy in mice reflects an insulin-sensitive reversible loss of nNOS. |
| 433 | 10930440 | Insulin restores neuronal nitric oxide synthase expression and function that is lost in diabetic gastropathy. |
| 434 | 10930440 | The decline of nNOS in diabetic mice does not result from loss of myenteric neurons. nNOS expression and pyloric function are restored to normal levels by insulin treatment. |
| 435 | 10930440 | Thus diabetic gastropathy in mice reflects an insulin-sensitive reversible loss of nNOS. |
| 436 | 10930440 | Insulin restores neuronal nitric oxide synthase expression and function that is lost in diabetic gastropathy. |
| 437 | 10930440 | The decline of nNOS in diabetic mice does not result from loss of myenteric neurons. nNOS expression and pyloric function are restored to normal levels by insulin treatment. |
| 438 | 10930440 | Thus diabetic gastropathy in mice reflects an insulin-sensitive reversible loss of nNOS. |
| 439 | 10945224 | This review will discuss the role of NO and nitric oxide synthase (NOS) in pathophysiologic and therapeutic implications in various autoimmune diseases with particular reference to T helper-1 (Th1) and T helper-2 (Th2) cytokines. |
| 440 | 10963118 | There was a decreased number of neurons containing nitric oxide synthase (NOS) in myenteric ganglia of antrum and duodenum. |
| 441 | 10963118 | There was no difference regarding neuropeptide Y (NPY) and galanin between diabetic and control mice; nor was there any difference between pre-diabetic NOD mice and controls regarding all bioactive substances investigated. |
| 442 | 10966937 | However, the contribution of nitric oxide synthase (NOS) isoforms to intrarenal production of NO in diabetes remains unknown. |
| 443 | 10969153 | Acetylcholine-induced relaxation was largely due to nitric oxide (NO)-mediated relaxation; however, a small but significant portion of relaxation in aortic rings from temocapril-treated diabetic rats was resistant to inhibition by the nitric oxide synthase (NOS) inhibitor, L-nitroarginine. |
| 444 | 10976915 | Regulation of myosin-bound protein phosphatase by insulin in vascular smooth muscle cells: evaluation of the role of Rho kinase and phosphatidylinositol-3-kinase-dependent signaling pathways. |
| 445 | 10976915 | Insulin-mediated MBP activation was accompanied by a rapid time-dependent reduction in the phosphorylation state of the myosin-bound regulatory subunit (MBS) of MBP. |
| 446 | 10976915 | The decrease observed in MBS phosphorylation was due to insulin-induced inhibition of Rho kinase activity. |
| 447 | 10976915 | Insulin also prevented a thrombin-mediated increase in Rho kinase activation and abolished the thrombin-induced increase in MBS phosphorylation and MBP inactivation. |
| 448 | 10976915 | These data are consistent with the notion that insulin inactivates Rho kinase and decreases MBS phosphorylation to activate MBP in VSMCs. |
| 449 | 10976915 | Furthermore, treatment with synthetic inhibitors of phosphatidylinositol-3 kinase (PI3-kinase), nitric oxide synthase (NOS), and cyclic guanosine monophosphate (cGMP) all blocked insulin's effect on MBP activation. |
| 450 | 10976915 | We conclude that insulin stimulates MBP via its regulatory subunit, MBS partly by inactivating Rho kinase and stimulating NO/cGMP signaling via PI3-kinase as part of a complex signaling network that controls 20-kDa myosin light chain (MLC20) phosphorylation and VSMC contraction. |
| 451 | 11043403 | The receptor tyrosine phosphatase-like protein ICA512 binds the PDZ domains of beta2-syntrophin and nNOS in pancreatic beta-cells. |
| 452 | 11043403 | Here we show that in a yeast two-hybrid assay its cytoplasmic domain binds beta2-syntrophin, a modular adapter which in muscle cells interacts with members of the dystrophin family including utrophin, as well as the signaling molecule neuronal nitric oxide synthase (nNOS). |
| 453 | 11043403 | This isoform included the PDZ domain, but not the C-terminal region, which in full-length beta2-syntrophin is responsible for binding dystrophin-related proteins. |
| 454 | 11043403 | In vitro binding of the beta2-syntrophin PDZ domain to ICA512 required both ICA512's C-terminal region and an internal polypeptide preceding its tyrosine phosphatase-like domain. |
| 455 | 11043403 | ICA512 also interacted in vitro with the PDZ domain of nNOS and ICA512-nNOS complexes were co-immunoprecipitated from INS-1 cells. |
| 456 | 11043403 | Thus, we propose that ICA512, through beta2-syntrophin and nNOS, links secretory granules with the actin cytoskeleton and signaling pathways involving nitric oxide. |
| 457 | 11043403 | The receptor tyrosine phosphatase-like protein ICA512 binds the PDZ domains of beta2-syntrophin and nNOS in pancreatic beta-cells. |
| 458 | 11043403 | Here we show that in a yeast two-hybrid assay its cytoplasmic domain binds beta2-syntrophin, a modular adapter which in muscle cells interacts with members of the dystrophin family including utrophin, as well as the signaling molecule neuronal nitric oxide synthase (nNOS). |
| 459 | 11043403 | This isoform included the PDZ domain, but not the C-terminal region, which in full-length beta2-syntrophin is responsible for binding dystrophin-related proteins. |
| 460 | 11043403 | In vitro binding of the beta2-syntrophin PDZ domain to ICA512 required both ICA512's C-terminal region and an internal polypeptide preceding its tyrosine phosphatase-like domain. |
| 461 | 11043403 | ICA512 also interacted in vitro with the PDZ domain of nNOS and ICA512-nNOS complexes were co-immunoprecipitated from INS-1 cells. |
| 462 | 11043403 | Thus, we propose that ICA512, through beta2-syntrophin and nNOS, links secretory granules with the actin cytoskeleton and signaling pathways involving nitric oxide. |
| 463 | 11043403 | The receptor tyrosine phosphatase-like protein ICA512 binds the PDZ domains of beta2-syntrophin and nNOS in pancreatic beta-cells. |
| 464 | 11043403 | Here we show that in a yeast two-hybrid assay its cytoplasmic domain binds beta2-syntrophin, a modular adapter which in muscle cells interacts with members of the dystrophin family including utrophin, as well as the signaling molecule neuronal nitric oxide synthase (nNOS). |
| 465 | 11043403 | This isoform included the PDZ domain, but not the C-terminal region, which in full-length beta2-syntrophin is responsible for binding dystrophin-related proteins. |
| 466 | 11043403 | In vitro binding of the beta2-syntrophin PDZ domain to ICA512 required both ICA512's C-terminal region and an internal polypeptide preceding its tyrosine phosphatase-like domain. |
| 467 | 11043403 | ICA512 also interacted in vitro with the PDZ domain of nNOS and ICA512-nNOS complexes were co-immunoprecipitated from INS-1 cells. |
| 468 | 11043403 | Thus, we propose that ICA512, through beta2-syntrophin and nNOS, links secretory granules with the actin cytoskeleton and signaling pathways involving nitric oxide. |
| 469 | 11043403 | The receptor tyrosine phosphatase-like protein ICA512 binds the PDZ domains of beta2-syntrophin and nNOS in pancreatic beta-cells. |
| 470 | 11043403 | Here we show that in a yeast two-hybrid assay its cytoplasmic domain binds beta2-syntrophin, a modular adapter which in muscle cells interacts with members of the dystrophin family including utrophin, as well as the signaling molecule neuronal nitric oxide synthase (nNOS). |
| 471 | 11043403 | This isoform included the PDZ domain, but not the C-terminal region, which in full-length beta2-syntrophin is responsible for binding dystrophin-related proteins. |
| 472 | 11043403 | In vitro binding of the beta2-syntrophin PDZ domain to ICA512 required both ICA512's C-terminal region and an internal polypeptide preceding its tyrosine phosphatase-like domain. |
| 473 | 11043403 | ICA512 also interacted in vitro with the PDZ domain of nNOS and ICA512-nNOS complexes were co-immunoprecipitated from INS-1 cells. |
| 474 | 11043403 | Thus, we propose that ICA512, through beta2-syntrophin and nNOS, links secretory granules with the actin cytoskeleton and signaling pathways involving nitric oxide. |
| 475 | 11050665 | Removal of oxygen species by incubating pancreatic tissues in the presence of polyethylene glycol-conjugated superoxide dismutase (PEG-SOD) (1 U/ml) produced a decrease in nitrite levels (42%) and NO synthase (NOS) activity (50%) in diabetic but not in control samples. |
| 476 | 11050665 | Moreover, inhibition of NOS activity produces an increase in SOD activity and a decrease in lipoperoxidation in diabetic pancreatic tissues. |
| 477 | 11050665 | Removal of oxygen species by incubating pancreatic tissues in the presence of polyethylene glycol-conjugated superoxide dismutase (PEG-SOD) (1 U/ml) produced a decrease in nitrite levels (42%) and NO synthase (NOS) activity (50%) in diabetic but not in control samples. |
| 478 | 11050665 | Moreover, inhibition of NOS activity produces an increase in SOD activity and a decrease in lipoperoxidation in diabetic pancreatic tissues. |
| 479 | 11087959 | Activation of hypothalamic neuronal nitric oxide synthase in lithium-induced diabetes insipidus rats. |
| 480 | 11087959 | The expression of the neuronal nitric oxide synthase (nNOS) gene in the paraventricular (PVN) and supraoptic nuclei (SON) in rats with lithium (Li)-induced polyuria was examined by using in situ hybridization histochemistry. |
| 481 | 11087959 | The state of the thyroid axis in these rats was also examined by in situ hybridization histochemistry for thyrotropin-releasing hormone (TRH) and thyroid-stimulating hormone (TSH) mRNAs and radioimmunoassay for circulating thyroid hormones. |
| 482 | 11087959 | The nNOS mRNA in the PVN and SON was significantly increased in the Li-treated rats in comparison with that in control. |
| 483 | 11087959 | The increased levels of the nNOS mRNA in the PVN and SON were confirmed by NADPH-diaphorase histochemical staining. |
| 484 | 11087959 | These results suggest that Li-induced diabetes insipidus may activate nNOS in the PVN and SON without change of the thyroid axis. |
| 485 | 11087959 | Activation of hypothalamic neuronal nitric oxide synthase in lithium-induced diabetes insipidus rats. |
| 486 | 11087959 | The expression of the neuronal nitric oxide synthase (nNOS) gene in the paraventricular (PVN) and supraoptic nuclei (SON) in rats with lithium (Li)-induced polyuria was examined by using in situ hybridization histochemistry. |
| 487 | 11087959 | The state of the thyroid axis in these rats was also examined by in situ hybridization histochemistry for thyrotropin-releasing hormone (TRH) and thyroid-stimulating hormone (TSH) mRNAs and radioimmunoassay for circulating thyroid hormones. |
| 488 | 11087959 | The nNOS mRNA in the PVN and SON was significantly increased in the Li-treated rats in comparison with that in control. |
| 489 | 11087959 | The increased levels of the nNOS mRNA in the PVN and SON were confirmed by NADPH-diaphorase histochemical staining. |
| 490 | 11087959 | These results suggest that Li-induced diabetes insipidus may activate nNOS in the PVN and SON without change of the thyroid axis. |
| 491 | 11087959 | Activation of hypothalamic neuronal nitric oxide synthase in lithium-induced diabetes insipidus rats. |
| 492 | 11087959 | The expression of the neuronal nitric oxide synthase (nNOS) gene in the paraventricular (PVN) and supraoptic nuclei (SON) in rats with lithium (Li)-induced polyuria was examined by using in situ hybridization histochemistry. |
| 493 | 11087959 | The state of the thyroid axis in these rats was also examined by in situ hybridization histochemistry for thyrotropin-releasing hormone (TRH) and thyroid-stimulating hormone (TSH) mRNAs and radioimmunoassay for circulating thyroid hormones. |
| 494 | 11087959 | The nNOS mRNA in the PVN and SON was significantly increased in the Li-treated rats in comparison with that in control. |
| 495 | 11087959 | The increased levels of the nNOS mRNA in the PVN and SON were confirmed by NADPH-diaphorase histochemical staining. |
| 496 | 11087959 | These results suggest that Li-induced diabetes insipidus may activate nNOS in the PVN and SON without change of the thyroid axis. |
| 497 | 11087959 | Activation of hypothalamic neuronal nitric oxide synthase in lithium-induced diabetes insipidus rats. |
| 498 | 11087959 | The expression of the neuronal nitric oxide synthase (nNOS) gene in the paraventricular (PVN) and supraoptic nuclei (SON) in rats with lithium (Li)-induced polyuria was examined by using in situ hybridization histochemistry. |
| 499 | 11087959 | The state of the thyroid axis in these rats was also examined by in situ hybridization histochemistry for thyrotropin-releasing hormone (TRH) and thyroid-stimulating hormone (TSH) mRNAs and radioimmunoassay for circulating thyroid hormones. |
| 500 | 11087959 | The nNOS mRNA in the PVN and SON was significantly increased in the Li-treated rats in comparison with that in control. |
| 501 | 11087959 | The increased levels of the nNOS mRNA in the PVN and SON were confirmed by NADPH-diaphorase histochemical staining. |
| 502 | 11087959 | These results suggest that Li-induced diabetes insipidus may activate nNOS in the PVN and SON without change of the thyroid axis. |
| 503 | 11087959 | Activation of hypothalamic neuronal nitric oxide synthase in lithium-induced diabetes insipidus rats. |
| 504 | 11087959 | The expression of the neuronal nitric oxide synthase (nNOS) gene in the paraventricular (PVN) and supraoptic nuclei (SON) in rats with lithium (Li)-induced polyuria was examined by using in situ hybridization histochemistry. |
| 505 | 11087959 | The state of the thyroid axis in these rats was also examined by in situ hybridization histochemistry for thyrotropin-releasing hormone (TRH) and thyroid-stimulating hormone (TSH) mRNAs and radioimmunoassay for circulating thyroid hormones. |
| 506 | 11087959 | The nNOS mRNA in the PVN and SON was significantly increased in the Li-treated rats in comparison with that in control. |
| 507 | 11087959 | The increased levels of the nNOS mRNA in the PVN and SON were confirmed by NADPH-diaphorase histochemical staining. |
| 508 | 11087959 | These results suggest that Li-induced diabetes insipidus may activate nNOS in the PVN and SON without change of the thyroid axis. |
| 509 | 11111015 | The permeability in the intact and diabetic rat coronary circulation after administration of secretin (3.0 micromol/kg i.v.), an inhibitor of NOS (nitric oxide synthase), and L-NAME (N(G)-nitro-L-arginine-methyl ester hydrochloride) (1 mg/kg i.v.), and both substances given together, were studied. |
| 510 | 11157681 | Incubation of endothelial cells in vitro with high concentrations of glucose activates protein kinase C (PKC) and increases nitric oxide synthase (NOS III) gene expression as well as superoxide production. |
| 511 | 11157681 | Similarly, we found an activation of the NADPH oxidase and a 7-fold increase in gp91(phox) mRNA in diabetic vessels. |
| 512 | 11160605 | Experiments were performed to investigate whether nitric-oxide synthase (NOS) activity can be detected in vascular smooth muscle (VSM) from 12- to 14-week streptozotocin (STZ)-diabetic rats. |
| 513 | 11160605 | The selective iNOS inhibitor S-ethylisothiourea (EIT), but not the selective nNOS inhibitor 7-nitroindazole (7-NINA), produced an increase in the NE pD2 value in endothelium-denuded mesenteric arteries from diabetic but not control rats. |
| 514 | 11160605 | Immunohistochemical staining indicated the presence of iNOS (but not eNOS or nNOS) in the medial and adventitial layers of mesenteric arteries from diabetic but not control rats. |
| 515 | 11160605 | Quantitative measurement of cytosolic NOS activity indicated no significant calcium-dependent (nNOS) activity in control or diabetic arteries, or calcium-independent (iNOS) activity in control arteries. |
| 516 | 11160605 | Experiments were performed to investigate whether nitric-oxide synthase (NOS) activity can be detected in vascular smooth muscle (VSM) from 12- to 14-week streptozotocin (STZ)-diabetic rats. |
| 517 | 11160605 | The selective iNOS inhibitor S-ethylisothiourea (EIT), but not the selective nNOS inhibitor 7-nitroindazole (7-NINA), produced an increase in the NE pD2 value in endothelium-denuded mesenteric arteries from diabetic but not control rats. |
| 518 | 11160605 | Immunohistochemical staining indicated the presence of iNOS (but not eNOS or nNOS) in the medial and adventitial layers of mesenteric arteries from diabetic but not control rats. |
| 519 | 11160605 | Quantitative measurement of cytosolic NOS activity indicated no significant calcium-dependent (nNOS) activity in control or diabetic arteries, or calcium-independent (iNOS) activity in control arteries. |
| 520 | 11160605 | Experiments were performed to investigate whether nitric-oxide synthase (NOS) activity can be detected in vascular smooth muscle (VSM) from 12- to 14-week streptozotocin (STZ)-diabetic rats. |
| 521 | 11160605 | The selective iNOS inhibitor S-ethylisothiourea (EIT), but not the selective nNOS inhibitor 7-nitroindazole (7-NINA), produced an increase in the NE pD2 value in endothelium-denuded mesenteric arteries from diabetic but not control rats. |
| 522 | 11160605 | Immunohistochemical staining indicated the presence of iNOS (but not eNOS or nNOS) in the medial and adventitial layers of mesenteric arteries from diabetic but not control rats. |
| 523 | 11160605 | Quantitative measurement of cytosolic NOS activity indicated no significant calcium-dependent (nNOS) activity in control or diabetic arteries, or calcium-independent (iNOS) activity in control arteries. |
| 524 | 11160605 | Experiments were performed to investigate whether nitric-oxide synthase (NOS) activity can be detected in vascular smooth muscle (VSM) from 12- to 14-week streptozotocin (STZ)-diabetic rats. |
| 525 | 11160605 | The selective iNOS inhibitor S-ethylisothiourea (EIT), but not the selective nNOS inhibitor 7-nitroindazole (7-NINA), produced an increase in the NE pD2 value in endothelium-denuded mesenteric arteries from diabetic but not control rats. |
| 526 | 11160605 | Immunohistochemical staining indicated the presence of iNOS (but not eNOS or nNOS) in the medial and adventitial layers of mesenteric arteries from diabetic but not control rats. |
| 527 | 11160605 | Quantitative measurement of cytosolic NOS activity indicated no significant calcium-dependent (nNOS) activity in control or diabetic arteries, or calcium-independent (iNOS) activity in control arteries. |
| 528 | 11179606 | Orexin-A immunoreactive neurons in the rat hypothalamus do not contain neuronal nitric oxide synthase (nNOS). |
| 529 | 11179606 | In this study, we used immunohistochemistry to investigate the possibility that rat LHA neurons co-express orexin-A and neuronal nitric oxide synthase (nNOS). |
| 530 | 11179606 | The orexin-A and nNOS cell populations in the LHA showed extensive overlap without co-localization, and no evidence of direct anatomic contact was found. |
| 531 | 11179606 | The finding that LHA neurons do not co-localize orexin-A and nNOS may suggest that the actions of the orexins and nitric oxide on food intake are mediated via independent mechanisms, however, nitric oxide is a diffusible molecule and could potentially affect the activity of orexin neurons via a non-synaptic mechanism. |
| 532 | 11179606 | Orexin-A immunoreactive neurons in the rat hypothalamus do not contain neuronal nitric oxide synthase (nNOS). |
| 533 | 11179606 | In this study, we used immunohistochemistry to investigate the possibility that rat LHA neurons co-express orexin-A and neuronal nitric oxide synthase (nNOS). |
| 534 | 11179606 | The orexin-A and nNOS cell populations in the LHA showed extensive overlap without co-localization, and no evidence of direct anatomic contact was found. |
| 535 | 11179606 | The finding that LHA neurons do not co-localize orexin-A and nNOS may suggest that the actions of the orexins and nitric oxide on food intake are mediated via independent mechanisms, however, nitric oxide is a diffusible molecule and could potentially affect the activity of orexin neurons via a non-synaptic mechanism. |
| 536 | 11179606 | Orexin-A immunoreactive neurons in the rat hypothalamus do not contain neuronal nitric oxide synthase (nNOS). |
| 537 | 11179606 | In this study, we used immunohistochemistry to investigate the possibility that rat LHA neurons co-express orexin-A and neuronal nitric oxide synthase (nNOS). |
| 538 | 11179606 | The orexin-A and nNOS cell populations in the LHA showed extensive overlap without co-localization, and no evidence of direct anatomic contact was found. |
| 539 | 11179606 | The finding that LHA neurons do not co-localize orexin-A and nNOS may suggest that the actions of the orexins and nitric oxide on food intake are mediated via independent mechanisms, however, nitric oxide is a diffusible molecule and could potentially affect the activity of orexin neurons via a non-synaptic mechanism. |
| 540 | 11179606 | Orexin-A immunoreactive neurons in the rat hypothalamus do not contain neuronal nitric oxide synthase (nNOS). |
| 541 | 11179606 | In this study, we used immunohistochemistry to investigate the possibility that rat LHA neurons co-express orexin-A and neuronal nitric oxide synthase (nNOS). |
| 542 | 11179606 | The orexin-A and nNOS cell populations in the LHA showed extensive overlap without co-localization, and no evidence of direct anatomic contact was found. |
| 543 | 11179606 | The finding that LHA neurons do not co-localize orexin-A and nNOS may suggest that the actions of the orexins and nitric oxide on food intake are mediated via independent mechanisms, however, nitric oxide is a diffusible molecule and could potentially affect the activity of orexin neurons via a non-synaptic mechanism. |
| 544 | 11193191 | The volume density of nitric oxide synthase (NOS)-IR nerve fibres was decreased in antrum and duodenum of diabetic mice, whereas no difference was found in colon. |
| 545 | 11193191 | Whereas neuropeptide Y (NPY)- and vesicular acetylcholine transporter (VAChT)-IR nerve fibres was increased in density in colon of diabetic mice, no difference was found in antrum and duodenum. |
| 546 | 11205877 | Insulin restores neuronal nitric oxide synthase expression in streptozotocin-induced diabetic rats. |
| 547 | 11205877 | Nitric oxide (NO) is known to play an important role in the pathophysiology of insulin-dependent diabetic mellitus (IDDM). |
| 548 | 11205877 | In an attempt to investigate the relation between insulin and NO in IDDM, the present study employed male Wistar rats to induce IDDM by intravenous injection of streptozotocin (STZ). |
| 549 | 11205877 | Insulin treatment reversed the nNOS activity. |
| 550 | 11205877 | Similar reversion by insulin treatment was also obtained in the gene expression of nNOS. |
| 551 | 11205877 | These findings indicated that an impairment of nNOS in the brain of rats with IDDM is mainly due to the absence of insulin. |
| 552 | 11205877 | Insulin restores neuronal nitric oxide synthase expression in streptozotocin-induced diabetic rats. |
| 553 | 11205877 | Nitric oxide (NO) is known to play an important role in the pathophysiology of insulin-dependent diabetic mellitus (IDDM). |
| 554 | 11205877 | In an attempt to investigate the relation between insulin and NO in IDDM, the present study employed male Wistar rats to induce IDDM by intravenous injection of streptozotocin (STZ). |
| 555 | 11205877 | Insulin treatment reversed the nNOS activity. |
| 556 | 11205877 | Similar reversion by insulin treatment was also obtained in the gene expression of nNOS. |
| 557 | 11205877 | These findings indicated that an impairment of nNOS in the brain of rats with IDDM is mainly due to the absence of insulin. |
| 558 | 11205877 | Insulin restores neuronal nitric oxide synthase expression in streptozotocin-induced diabetic rats. |
| 559 | 11205877 | Nitric oxide (NO) is known to play an important role in the pathophysiology of insulin-dependent diabetic mellitus (IDDM). |
| 560 | 11205877 | In an attempt to investigate the relation between insulin and NO in IDDM, the present study employed male Wistar rats to induce IDDM by intravenous injection of streptozotocin (STZ). |
| 561 | 11205877 | Insulin treatment reversed the nNOS activity. |
| 562 | 11205877 | Similar reversion by insulin treatment was also obtained in the gene expression of nNOS. |
| 563 | 11205877 | These findings indicated that an impairment of nNOS in the brain of rats with IDDM is mainly due to the absence of insulin. |
| 564 | 11205877 | Insulin restores neuronal nitric oxide synthase expression in streptozotocin-induced diabetic rats. |
| 565 | 11205877 | Nitric oxide (NO) is known to play an important role in the pathophysiology of insulin-dependent diabetic mellitus (IDDM). |
| 566 | 11205877 | In an attempt to investigate the relation between insulin and NO in IDDM, the present study employed male Wistar rats to induce IDDM by intravenous injection of streptozotocin (STZ). |
| 567 | 11205877 | Insulin treatment reversed the nNOS activity. |
| 568 | 11205877 | Similar reversion by insulin treatment was also obtained in the gene expression of nNOS. |
| 569 | 11205877 | These findings indicated that an impairment of nNOS in the brain of rats with IDDM is mainly due to the absence of insulin. |
| 570 | 11272132 | To determine if the mechanism leading to NO-stimulated glucose uptake is similar to the insulin- or contraction-dependent signaling pathways, isolated soleus and extensor digitorum longus (EDL) muscles from rats were treated with various combinations of SNP (maximum 10 mmol/l), insulin (maximum 50 mU/ml), electrical stimulation to produce contractions (maximum 10 min), wortmannin (100 nmol/l), and/or the NO synthase (NOS) inhibitor NG-monomethyl-L-arginine (L-NMMA) (0.1 mmol/l). |
| 571 | 11323020 | NO is produced through L-arginine pathway by three different isoforms of nitric oxide synthase (NOS), an inducible form that can be activated by cytokines such as tumor necrosis factor alpha (TNFalpha). |
| 572 | 11323020 | We evaluated NO plasmatic levels, endothelial damage markers such as von Willebrand factor (vWF), platelet activation, soluble P-selectin (sP-Sel), TNFalpha levels, insulinaemia (I), glycosylated haemoglobin (HbA1c), glycaemia and blood pressure in 32 hypertensive diabetic type II patients (Group A), 37 hypertensive patients (Group B) and 35 healthy subjects (Group C) matched in sex, age, body mass index and dietary habits. |
| 573 | 11323020 | These parameters described a prothrombotic state associated with an insulin resistance state, an increased vWF release, raised sP-Sel and TNFalpha levels and, maybe, low NO bioavailability, which could lead to a higher risk of development of thrombotic events in hypertensive diabetic patients (Group A) than in the hypertensive patients in Group B. |
| 574 | 11337908 | NO synthase (NOS) catalyses the conversion of L-arginine to L-citrulline in the presence of oxygen and NADPH-diaphorase (NADPH-d). |
| 575 | 11337908 | In this study, we evaluated the expression of endothelial NOS (eNOS) enzyme and its co-enzyme in diabetic rat hearts. |
| 576 | 11337908 | NO synthase (NOS) catalyses the conversion of L-arginine to L-citrulline in the presence of oxygen and NADPH-diaphorase (NADPH-d). |
| 577 | 11337908 | In this study, we evaluated the expression of endothelial NOS (eNOS) enzyme and its co-enzyme in diabetic rat hearts. |
| 578 | 11350073 | NO is synthesized by nitric oxide synthase (NOS). |
| 579 | 11368236 | Since nitric oxide (NO)-mediated effects on cardiovascular dynamics are altered in diabetes, we evaluated the effect of L-NAME, a nitric oxide synthase (NOS) antagonist, on mean arterial pressure (MAP), heart rate (HR), and selective vascular flows in both male and female normal and diabetic rats as an index of NO activity. |
| 580 | 11375331 | A neuronal isoform of nitric oxide synthase expressed in pancreatic beta-cells controls insulin secretion. |
| 581 | 11375331 | Evidence is presented showing that a neuronal isoform of nitric oxide synthase (NOS) is expressed in rat pancreatic islets and INS-1 cells. |
| 582 | 11375331 | Double-immunofluorescence studies demonstrated the presence of nNOS in insulin-secreting beta-cells. |
| 583 | 11375331 | Electron microscopy studies showed that nNOS was mainly localized in insulin secretory granules and to a lesser extent in the mitochondria and the nucleus. |
| 584 | 11375331 | Our data show that miconazole, an inhibitor of nNOS cytochrome c reductase activity, either alone for the experiments with arginine or combined with sodium nitroprusside for glucose, is able to restore normal secretory patterns in response to the two secretagogues. |
| 585 | 11375331 | Furthermore, these results were corroborated by the demonstration of a direct enzyme-substrate interaction between nNOS and cytochrome c, which is strongly reinforced in the presence of the NOS inhibitor. |
| 586 | 11375331 | A neuronal isoform of nitric oxide synthase expressed in pancreatic beta-cells controls insulin secretion. |
| 587 | 11375331 | Evidence is presented showing that a neuronal isoform of nitric oxide synthase (NOS) is expressed in rat pancreatic islets and INS-1 cells. |
| 588 | 11375331 | Double-immunofluorescence studies demonstrated the presence of nNOS in insulin-secreting beta-cells. |
| 589 | 11375331 | Electron microscopy studies showed that nNOS was mainly localized in insulin secretory granules and to a lesser extent in the mitochondria and the nucleus. |
| 590 | 11375331 | Our data show that miconazole, an inhibitor of nNOS cytochrome c reductase activity, either alone for the experiments with arginine or combined with sodium nitroprusside for glucose, is able to restore normal secretory patterns in response to the two secretagogues. |
| 591 | 11375331 | Furthermore, these results were corroborated by the demonstration of a direct enzyme-substrate interaction between nNOS and cytochrome c, which is strongly reinforced in the presence of the NOS inhibitor. |
| 592 | 11375331 | A neuronal isoform of nitric oxide synthase expressed in pancreatic beta-cells controls insulin secretion. |
| 593 | 11375331 | Evidence is presented showing that a neuronal isoform of nitric oxide synthase (NOS) is expressed in rat pancreatic islets and INS-1 cells. |
| 594 | 11375331 | Double-immunofluorescence studies demonstrated the presence of nNOS in insulin-secreting beta-cells. |
| 595 | 11375331 | Electron microscopy studies showed that nNOS was mainly localized in insulin secretory granules and to a lesser extent in the mitochondria and the nucleus. |
| 596 | 11375331 | Our data show that miconazole, an inhibitor of nNOS cytochrome c reductase activity, either alone for the experiments with arginine or combined with sodium nitroprusside for glucose, is able to restore normal secretory patterns in response to the two secretagogues. |
| 597 | 11375331 | Furthermore, these results were corroborated by the demonstration of a direct enzyme-substrate interaction between nNOS and cytochrome c, which is strongly reinforced in the presence of the NOS inhibitor. |
| 598 | 11375331 | A neuronal isoform of nitric oxide synthase expressed in pancreatic beta-cells controls insulin secretion. |
| 599 | 11375331 | Evidence is presented showing that a neuronal isoform of nitric oxide synthase (NOS) is expressed in rat pancreatic islets and INS-1 cells. |
| 600 | 11375331 | Double-immunofluorescence studies demonstrated the presence of nNOS in insulin-secreting beta-cells. |
| 601 | 11375331 | Electron microscopy studies showed that nNOS was mainly localized in insulin secretory granules and to a lesser extent in the mitochondria and the nucleus. |
| 602 | 11375331 | Our data show that miconazole, an inhibitor of nNOS cytochrome c reductase activity, either alone for the experiments with arginine or combined with sodium nitroprusside for glucose, is able to restore normal secretory patterns in response to the two secretagogues. |
| 603 | 11375331 | Furthermore, these results were corroborated by the demonstration of a direct enzyme-substrate interaction between nNOS and cytochrome c, which is strongly reinforced in the presence of the NOS inhibitor. |
| 604 | 11375331 | A neuronal isoform of nitric oxide synthase expressed in pancreatic beta-cells controls insulin secretion. |
| 605 | 11375331 | Evidence is presented showing that a neuronal isoform of nitric oxide synthase (NOS) is expressed in rat pancreatic islets and INS-1 cells. |
| 606 | 11375331 | Double-immunofluorescence studies demonstrated the presence of nNOS in insulin-secreting beta-cells. |
| 607 | 11375331 | Electron microscopy studies showed that nNOS was mainly localized in insulin secretory granules and to a lesser extent in the mitochondria and the nucleus. |
| 608 | 11375331 | Our data show that miconazole, an inhibitor of nNOS cytochrome c reductase activity, either alone for the experiments with arginine or combined with sodium nitroprusside for glucose, is able to restore normal secretory patterns in response to the two secretagogues. |
| 609 | 11375331 | Furthermore, these results were corroborated by the demonstration of a direct enzyme-substrate interaction between nNOS and cytochrome c, which is strongly reinforced in the presence of the NOS inhibitor. |
| 610 | 11384198 | Citrulline formed by the NOS reaction is recycled to arginine by the citrulline-NO cycle, which is composed of NOS, argininosuccinate synthetase (AS), and argininosuccinate lyase. |
| 611 | 11384198 | Cationic amino acid transporter (CAT)-1 mRNA remained little changed, and CAT-2 mRNA was not detected. |
| 612 | 11384198 | Transforming growth factor-beta1 (TGF-beta1) mRNA in the aorta was also induced. |
| 613 | 11384198 | TGF-beta1 induced eNOS and AS mRNAs in human umbilical vein endothelial cells but inhibited the proliferation of HUVEC. |
| 614 | 11384198 | These results indicate that eNOS and AS are coinduced in the aorta in early stages of STZ-induced diabetic rats and that the induction is mediated by TGF-beta1. |
| 615 | 11410636 | Gastric distension-induced pyloric relaxation was significantly reduced by subdiaphragmatic vagotomy, hexamethonium (20 mg kg(-1)) and N (G)-nitro-L-arginine methyl ester (L-NAME; 10 mg kg(-1)), a nitric oxide synthase (NOS) biosynthesis inhibitor, in anaesthetized rats. |
| 616 | 11426340 | Eight weeks later the animals were killed, the distal part of the vagina was removed, and smooth muscle strips were prepared for functional organ bath experiments and for measurement of nitric oxide synthase (NOS) activity. |
| 617 | 11426340 | SNAP and CGRP concentration-dependently inhibited EFS evoked contractions in both NDM and DM preparations. |
| 618 | 11445827 | The renal excretory responses to volume expansion (VE), by 10 % body wt, were determined in groups of anaesthetised streptozotocin-induced diabetic rats with one denervated and one innervated kidney in the presence and absence of nitric oxide synthase (NOS) inhibitors. |
| 619 | 11455192 | Nitric oxide synthase (NOS) activity was also evaluated. |
| 620 | 11455192 | In the SHAM group, HG exerted diabetes-like contractile dysfunctions, including depressed PS, prolonged TR90, reduced fluorescence intensity, higher tau and enhanced NOS activity when compared to myocytes maintained in low [glucose] medium (5.5 mM). |
| 621 | 11455192 | Interestingly, the HG- induced mechanical alterations were significantly exaggerated (TPS, TR90 and tau), reversed (PS and NOS) or lost (+/- dL/dt and fluorescence intensity) in the OVX group. |
| 622 | 11455192 | Nitric oxide synthase (NOS) activity was also evaluated. |
| 623 | 11455192 | In the SHAM group, HG exerted diabetes-like contractile dysfunctions, including depressed PS, prolonged TR90, reduced fluorescence intensity, higher tau and enhanced NOS activity when compared to myocytes maintained in low [glucose] medium (5.5 mM). |
| 624 | 11455192 | Interestingly, the HG- induced mechanical alterations were significantly exaggerated (TPS, TR90 and tau), reversed (PS and NOS) or lost (+/- dL/dt and fluorescence intensity) in the OVX group. |
| 625 | 11455192 | Nitric oxide synthase (NOS) activity was also evaluated. |
| 626 | 11455192 | In the SHAM group, HG exerted diabetes-like contractile dysfunctions, including depressed PS, prolonged TR90, reduced fluorescence intensity, higher tau and enhanced NOS activity when compared to myocytes maintained in low [glucose] medium (5.5 mM). |
| 627 | 11455192 | Interestingly, the HG- induced mechanical alterations were significantly exaggerated (TPS, TR90 and tau), reversed (PS and NOS) or lost (+/- dL/dt and fluorescence intensity) in the OVX group. |
| 628 | 11469395 | These beneficial effects may involve a decrease in early glycation products and/or nitric oxide synthase (NOS) activity. |
| 629 | 11514262 | Tetrahydrobiopterin is one of the most potent naturally occurring reducing agents and an essential cofactor required for enzymatic activity of nitric oxide synthase (NOS). |
| 630 | 11528370 | Systemic inhibition of nitric oxide synthase (NOS) in streptozotocin-induced (STZ-induced) diabetic rats results in decreases in glomerular filtration rate (GFR) and renal plasma flow (RPF) and an increase in renal vascular resistance (RVR). |
| 631 | 11550802 | The expression of nitric oxide synthase (NOS) isoforms I, III and protein kinase-Ctheta (PKCtheta) in rat vastus lateralis muscle was demonstrated immunohistochemically and then correlated to the physiological metabolic fibre types: SO (slow-oxidative), FOGI, FOGII (fast-oxidative glycolytic; I more glycolytic, II more oxidative), and FG (fast-glycolytic). |
| 632 | 11571673 | Here we evaluated the effect of nitric oxide synthase (NOS) inhibitors on the bone particle resorbing activity and TNF-alpha release of cultured peripheral blood monocytes (PBM) obtained from 10 premenopausal (PreM) and 10 postmenopausal (PostM) women. |
| 633 | 11571673 | Based on these findings and on the evidence that estrogen stimulates NOS, we suggest that estrogen withdrawal may reduce the inhibitory effect of NO on TNF-alpha release. |
| 634 | 11571673 | Here we evaluated the effect of nitric oxide synthase (NOS) inhibitors on the bone particle resorbing activity and TNF-alpha release of cultured peripheral blood monocytes (PBM) obtained from 10 premenopausal (PreM) and 10 postmenopausal (PostM) women. |
| 635 | 11571673 | Based on these findings and on the evidence that estrogen stimulates NOS, we suggest that estrogen withdrawal may reduce the inhibitory effect of NO on TNF-alpha release. |
| 636 | 11751281 | Neither diabetes nor diabetes with insulin treatment had significant effects on serum testosterone levels or NOS isoform (nNOS, eNOS, and iNOS) protein content in penile homogenates, indicating that the changes found in erectile function were independent of such variables. |
| 637 | 11755899 | At various time intervals after induction of diabetes the neurons in the paraventricular- (PVN) and supraoptic- (SON) nucleus showed upregulated arginine vasopressin (AVP) and oxytocin (OXT) immunoexpression, being most pronounced at 2 weeks. |
| 638 | 11755899 | This is coupled by upregulation of NMDAR1 and nNOS but downregulation of GluR2/3. |
| 639 | 11872364 | In particular, we discuss: (i) the insulin ability to rapidly activate a constitutive nitric oxide synthase (NOS) in both cell types, with a consequent increase of the two nucleotides guanosine-3',5'-cyclic monophosphate (cGMP) and adenosine-3',5'-cyclic monophosphate (cAMP), well-known mediators of antiaggregation and vasodilation; (ii) the interplay of insulin with substances able to activate adenylate cyclase in both cell types; (iii) the impairment of the antiaggregating insulin effects in insulin-resistant subjects; (iv) the insulin-induced increase on endothelin in the VSMCs; (v) the insulin ability to slightly stimulate VSMC proliferation. |
| 640 | 11879808 | We examined in vivo responses of the basilar artery in male and female nondiabetic and diabetic rats in response to a nitric oxide synthase (NOS)-dependent (acetylcholine) and -independent (nitroglycerin) agonist. |
| 641 | 11901190 | We present here the first evidence that peroxynitrite (ONOO(-)) releases zinc from the zinc-thiolate cluster of endothelial NOS (eNOS) and presumably forms disulfide bonds between the monomers. |
| 642 | 11901190 | Furthermore, eNOS derived from endothelial cells exposed to elevated glucose produces more O(2)(.-), and, like eNOS purified from diabetic LDL receptor-deficient mice, contains less zinc and fewer SDS-resistant dimers. |
| 643 | 11973412 | Muscarinic agonists produce endothelium-dependent vasodilatation in the presence of nitric oxide synthase (NOS) inhibition. |
| 644 | 11991635 | The aim of this study was to determine the effects of streptozotocin (STZ)-induced diabetes on nitric oxide (NO) metabolites in plasma and cerebellar nitric oxide synthase (NOS) activity. |
| 645 | 12031529 | Neuronal nitric oxide synthase (nNOS), tyrosine hydroxylase (TH), the immediate early gene c-Jun, vasoactive intestinal peptide (VIP) and calcitonin gene related peptide (CGRP) content and expression were measured in nodose ganglia of control, diabetic, and diabetic+insulin-treated rats using immunocytochemistry and reverse transcription-polymerase chain reaction (RT-PCR). |
| 646 | 12031529 | Moreover, no alterations in the numbers of vagal efferent NOS-containing neurons (labeled with NADPH-diaphorase histochemistry) were noted in the dorsal motor nucleus of the vagus (DMV) or the nucleus ambiguous (NA) of control, diabetic, and diabetic+insulin-treated rats at any time point. |
| 647 | 12031529 | The number of nodose ganglion neurons labeled for the protooncogene, c-Jun, was small yet slightly increased in the diabetic nodose ganglia at the 8-week time point and was reversed with insulin treatment. |
| 648 | 12031529 | Neuronal nitric oxide synthase (nNOS), tyrosine hydroxylase (TH), the immediate early gene c-Jun, vasoactive intestinal peptide (VIP) and calcitonin gene related peptide (CGRP) content and expression were measured in nodose ganglia of control, diabetic, and diabetic+insulin-treated rats using immunocytochemistry and reverse transcription-polymerase chain reaction (RT-PCR). |
| 649 | 12031529 | Moreover, no alterations in the numbers of vagal efferent NOS-containing neurons (labeled with NADPH-diaphorase histochemistry) were noted in the dorsal motor nucleus of the vagus (DMV) or the nucleus ambiguous (NA) of control, diabetic, and diabetic+insulin-treated rats at any time point. |
| 650 | 12031529 | The number of nodose ganglion neurons labeled for the protooncogene, c-Jun, was small yet slightly increased in the diabetic nodose ganglia at the 8-week time point and was reversed with insulin treatment. |
| 651 | 12074839 | Glucose-induced increase in NOx was eliminated by 0.1 mM L-nitro-arginine methylester (L-NAME), a nitric oxide synthase (NOS) inhibitor. |
| 652 | 12080716 | To study the relationship between nitric oxide(NO) and oxygen free radicals in rat kidney of diabetes mellitus(DM), the authors examined the changes of renal tissue NO level and nitric oxide synthase(NOS) activity, lipid peroxidation(LPO) level and superoxide dismutase(SOD), peroxidase(POD) and catalase (CAT) activities in streptozotocin(STZ)-induced diabetic rats and normal controls(NC) at the 2nd, 8th- and 16th-week. |
| 653 | 12092006 | This structural remodeling was accompanied by significantly decreased activity of endothelial nitric oxide synthase (NOS) and heterogeneously decreased activities of glycogen phosphorylase (GlPh), hydroxybutyrate dehydrogenase (HBDH) and adenosine triphophatases (ATPases) throughout the myocardium. |
| 654 | 12110512 | Endothelial nitric oxide synthase (NOS) and neuronal NOS protein increased in proximal tubules of acidotic diabetic rats 3-5 wk after streptozotocin injection. |
| 655 | 12171250 | The content of neuronal nitric oxide synthase (nNOS) in the colon and the caecum from pigs infected with Schistosoma japonicum was studied using immunohistochemical and histochemical staining for nNOS and nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-diaphorase), respectively. |
| 656 | 12171250 | In the infected pigs, lightly, moderately and less severely inflamed tissues showed increased nNOS and NADPH-diaphorase activities in nerve cell bodies and nerve fibres in the enteric plexuses compared to control pigs. |
| 657 | 12171250 | The content of neuronal nitric oxide synthase (nNOS) in the colon and the caecum from pigs infected with Schistosoma japonicum was studied using immunohistochemical and histochemical staining for nNOS and nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-diaphorase), respectively. |
| 658 | 12171250 | In the infected pigs, lightly, moderately and less severely inflamed tissues showed increased nNOS and NADPH-diaphorase activities in nerve cell bodies and nerve fibres in the enteric plexuses compared to control pigs. |
| 659 | 12191972 | This study examined the renal expression of the endothelial (eNOS), neuronal (nNOS), and inducible (iNOS) isoforms by both immunohistochemistry and Western blot analyses in sham-operated rats (S) and in rats subjected to 5/6 nephrectomy (Nx). |
| 660 | 12208472 | After the incubation the following parameters were evaluated: endothelial cell nitric oxide synthase (NOS) activity, nitric oxide (NO) and peroxynitrite production, Na(+)/K(+)-ATPase and Ca(2+)-ATPase activities, intracellular Ca(2+) concentration and fluidity of the superficial part of the plasma membrane studied by 1-(4-trimethylaminophenyl)-6-phenyl-1,3,5-hexatriene (TMA-DPH). |
| 661 | 12231652 | Using laser Doppler flowmetry, vasodilatory responses to acetylcholine (ACh; 0.1 mM) and morpholino-sydnonimine (SIN-1) were determined in the presence of Ringer solution, during inhibition of NO synthase (NOS) and cyclo-oxygenase (COX) with N(omega)-nitro-L-arginine (L-NNA; 1 mM) + indomethacin (10(-5) M), and during inhibition of K(+) channels, NOS and COX with tetraethylammonium (TEA; 10 mM) + L-NNA + indomethacin. |
| 662 | 12231652 | In age-matched controls, SIN-1-induced vasodilatation in the presence of TEA + L-NNA + indomethacin, basal NOS activity and the initial vasodilatory response to ACh during NOS and COX inhibition all decreased with maturation. |
| 663 | 12231652 | At 18-20 weeks of STZ-induced diabetes, ACh-induced vasodilatation during NOS and COX inhibition was prolonged due to increased K(+) channel activity and experimental diabetic sensory neuropathy (EDN) had developed. |
| 664 | 12231652 | Using laser Doppler flowmetry, vasodilatory responses to acetylcholine (ACh; 0.1 mM) and morpholino-sydnonimine (SIN-1) were determined in the presence of Ringer solution, during inhibition of NO synthase (NOS) and cyclo-oxygenase (COX) with N(omega)-nitro-L-arginine (L-NNA; 1 mM) + indomethacin (10(-5) M), and during inhibition of K(+) channels, NOS and COX with tetraethylammonium (TEA; 10 mM) + L-NNA + indomethacin. |
| 665 | 12231652 | In age-matched controls, SIN-1-induced vasodilatation in the presence of TEA + L-NNA + indomethacin, basal NOS activity and the initial vasodilatory response to ACh during NOS and COX inhibition all decreased with maturation. |
| 666 | 12231652 | At 18-20 weeks of STZ-induced diabetes, ACh-induced vasodilatation during NOS and COX inhibition was prolonged due to increased K(+) channel activity and experimental diabetic sensory neuropathy (EDN) had developed. |
| 667 | 12231652 | Using laser Doppler flowmetry, vasodilatory responses to acetylcholine (ACh; 0.1 mM) and morpholino-sydnonimine (SIN-1) were determined in the presence of Ringer solution, during inhibition of NO synthase (NOS) and cyclo-oxygenase (COX) with N(omega)-nitro-L-arginine (L-NNA; 1 mM) + indomethacin (10(-5) M), and during inhibition of K(+) channels, NOS and COX with tetraethylammonium (TEA; 10 mM) + L-NNA + indomethacin. |
| 668 | 12231652 | In age-matched controls, SIN-1-induced vasodilatation in the presence of TEA + L-NNA + indomethacin, basal NOS activity and the initial vasodilatory response to ACh during NOS and COX inhibition all decreased with maturation. |
| 669 | 12231652 | At 18-20 weeks of STZ-induced diabetes, ACh-induced vasodilatation during NOS and COX inhibition was prolonged due to increased K(+) channel activity and experimental diabetic sensory neuropathy (EDN) had developed. |
| 670 | 12233810 | Since the mid-1990s, nitric oxide synthase (NOS), the enzyme that catalyzes the formation of nitric oxide (NO) from L-arginine, has received considerable attention as a potential candidate for cardiovascular gene therapy, because NO exerts critical and diverse functions in the cardiovascular system, and abnormalities in NO biology are apparent in a number of cardiovascular disease processes including cerebral vasospasm, atherosclerosis, postangioplasty restenosis, transplant vasculopathy, hypertension, diabetes mellitus, impotence and delayed wound healing. |
| 671 | 12233810 | There are three NOS isoforms, i.e., endothelial (eNOS), neuronal (nNOS) and inducible (iNOS). |
| 672 | 12233810 | Since the mid-1990s, nitric oxide synthase (NOS), the enzyme that catalyzes the formation of nitric oxide (NO) from L-arginine, has received considerable attention as a potential candidate for cardiovascular gene therapy, because NO exerts critical and diverse functions in the cardiovascular system, and abnormalities in NO biology are apparent in a number of cardiovascular disease processes including cerebral vasospasm, atherosclerosis, postangioplasty restenosis, transplant vasculopathy, hypertension, diabetes mellitus, impotence and delayed wound healing. |
| 673 | 12233810 | There are three NOS isoforms, i.e., endothelial (eNOS), neuronal (nNOS) and inducible (iNOS). |
| 674 | 12378822 | Several pathways have been proposed as mechanisms for hyperglycemia-induced superoxide overproduction, including increased flux through the polyol pathway, depletion of nicotinamide adenine dinucleotide phosphate (NADPH), altered endogenous antioxidant enzymes, and reduced availability of tetrahydrobiopterin, an essential cofactor for nitric oxide synthase (NOS). |
| 675 | 12378824 | Thus, increasing cavernosal nitric oxide synthase (NOS) expression, cGMP levels and/or BKCa channel expression is an effective therapy for experimental ED. |
| 676 | 12419890 | In the present study, the effect of Folium mori on the expression of nitric oxide synthase (NOS) in the hypothalamus of STZ-induced diabetic rats was investigated via nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry. |
| 677 | 12425206 | The following review deals with relations of polymorphisms in the renin-angiotensin-aldosterone (RAAS) system, polymorphisms of NO-synthase (NOS) as well as the gene for atrial natriuretic peptide (hANP). |
| 678 | 12425206 | A relationship with the development of coronary disease was described in ACE genes, the receptor for angiotensin II--type 1 (AT1R), angiotensinogen and in several NOS polymorphisms. |
| 679 | 12425206 | Also the relationship of polymorphisms of genes ACE, AT1R, NOS and hANP was described in relation to the development of hypertension which is an important risk factor for macrovascular and microvascular complications of diabetes. |
| 680 | 12425206 | In some investigations the relationship of polymorphisms of ACE and AT1R genes and the development of diabetic nephropathy was described where a significant acceleration of the process of atherogenesis occurs. |
| 681 | 12425206 | The following review deals with relations of polymorphisms in the renin-angiotensin-aldosterone (RAAS) system, polymorphisms of NO-synthase (NOS) as well as the gene for atrial natriuretic peptide (hANP). |
| 682 | 12425206 | A relationship with the development of coronary disease was described in ACE genes, the receptor for angiotensin II--type 1 (AT1R), angiotensinogen and in several NOS polymorphisms. |
| 683 | 12425206 | Also the relationship of polymorphisms of genes ACE, AT1R, NOS and hANP was described in relation to the development of hypertension which is an important risk factor for macrovascular and microvascular complications of diabetes. |
| 684 | 12425206 | In some investigations the relationship of polymorphisms of ACE and AT1R genes and the development of diabetic nephropathy was described where a significant acceleration of the process of atherogenesis occurs. |
| 685 | 12425206 | The following review deals with relations of polymorphisms in the renin-angiotensin-aldosterone (RAAS) system, polymorphisms of NO-synthase (NOS) as well as the gene for atrial natriuretic peptide (hANP). |
| 686 | 12425206 | A relationship with the development of coronary disease was described in ACE genes, the receptor for angiotensin II--type 1 (AT1R), angiotensinogen and in several NOS polymorphisms. |
| 687 | 12425206 | Also the relationship of polymorphisms of genes ACE, AT1R, NOS and hANP was described in relation to the development of hypertension which is an important risk factor for macrovascular and microvascular complications of diabetes. |
| 688 | 12425206 | In some investigations the relationship of polymorphisms of ACE and AT1R genes and the development of diabetic nephropathy was described where a significant acceleration of the process of atherogenesis occurs. |
| 689 | 12432448 | Constitutive expression of nitric oxide synthase (NOS) II was found in rat hindlimb muscles by immunohistochemistry and western blotting during development from embryonic day 21 to the adult stage of 75 days. |
| 690 | 12536047 | In the present study, the effect of acupuncture on the expressions of neuronal nitric oxide synthase (nNOS) and nitric oxide synthase (NOS) in the dorsolateral periaqueductal gray (DL-PAG) area of rats with streptozotocin (STZ)-induced diabetes was investigated via nNOS immunohistochemistry and nicotinamide adenine dinucleotide phosphate-diaphorase histochemistry. |
| 691 | 12617792 | The uterine enzymatic activity in diabetic animals decreases in the presence of the NOS inhibitor NG-nitro-L-arginine methyl ester (P < 0.01) and is enhanced (P < 0.005) when a generating ROS system (xanthine/xanthine oxidase) is added to the incubating medium. |
| 692 | 12618307 | The aim of our study was to evaluate the effect of agmatine on allodynia in two experimental neuropathic pain models, the spinal nerve ligation (SNL) model and the streptozocin (STZ)-induced diabetic neuropathy in rats, and to determine if the N-methyl-D-aspartate (NMDA) receptor antagonists and the nitric oxide synthase (NOS) inhibitors influence this effect of agmatine. |
| 693 | 12624601 | The phlorizin-treated diabetic rats showed a significant decrease in the ratio of nNOS to beta-actin mRNA compared with diabetic rats. |
| 694 | 12647267 | Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthase (NOS). |
| 695 | 12694302 | These factors include a variety of guanidino compounds (GCs), which have been shown to be nitric oxide synthase (NOS) modulators both in vitro and in vivo. |
| 696 | 12694308 | An overproduction of reactive oxygen species (ROS) may injure the endothelial cell membrane, inactivate NO, and cause oxidation of an essential cofactor of nitric oxide synthase (NOS). |
| 697 | 12797599 | In kidney, nitric oxide (NO) synthesized by nitric oxide synthase (NOS) regulates sodium and water excretion, and renal medullary blood flow. |
| 698 | 12797599 | The expression of constitutive NOS, endothelial NOS (eNOS) and neuronal NOS (nNOS), were assessed in kidney of the spontaneously hypertensive rat (SHR) and the normotensive Wistar Kyoto (WKY) rat by Western blot analysis and immunocytochemistry. |
| 699 | 12797599 | Neuronal NOS expression was observed in the cortex and eNOS was detected only in theinner medulla of both WKY and SHR. |
| 700 | 12797599 | In SHR, expression of eNOS was attenuated to 35.1 +/- 10.8%, while expression of nNOS was only 57.5 +/- 5.7% of the levels seen in WKY rat. |
| 701 | 12797599 | The decreased renal blood flow observed in SHR may be linked to a diminished expression of eNOS and nNOS, underscoring the importance of these enzymes in the pathophysiology and maintenance of genetic hypertension. |
| 702 | 12797599 | In kidney, nitric oxide (NO) synthesized by nitric oxide synthase (NOS) regulates sodium and water excretion, and renal medullary blood flow. |
| 703 | 12797599 | The expression of constitutive NOS, endothelial NOS (eNOS) and neuronal NOS (nNOS), were assessed in kidney of the spontaneously hypertensive rat (SHR) and the normotensive Wistar Kyoto (WKY) rat by Western blot analysis and immunocytochemistry. |
| 704 | 12797599 | Neuronal NOS expression was observed in the cortex and eNOS was detected only in theinner medulla of both WKY and SHR. |
| 705 | 12797599 | In SHR, expression of eNOS was attenuated to 35.1 +/- 10.8%, while expression of nNOS was only 57.5 +/- 5.7% of the levels seen in WKY rat. |
| 706 | 12797599 | The decreased renal blood flow observed in SHR may be linked to a diminished expression of eNOS and nNOS, underscoring the importance of these enzymes in the pathophysiology and maintenance of genetic hypertension. |
| 707 | 12797599 | In kidney, nitric oxide (NO) synthesized by nitric oxide synthase (NOS) regulates sodium and water excretion, and renal medullary blood flow. |
| 708 | 12797599 | The expression of constitutive NOS, endothelial NOS (eNOS) and neuronal NOS (nNOS), were assessed in kidney of the spontaneously hypertensive rat (SHR) and the normotensive Wistar Kyoto (WKY) rat by Western blot analysis and immunocytochemistry. |
| 709 | 12797599 | Neuronal NOS expression was observed in the cortex and eNOS was detected only in theinner medulla of both WKY and SHR. |
| 710 | 12797599 | In SHR, expression of eNOS was attenuated to 35.1 +/- 10.8%, while expression of nNOS was only 57.5 +/- 5.7% of the levels seen in WKY rat. |
| 711 | 12797599 | The decreased renal blood flow observed in SHR may be linked to a diminished expression of eNOS and nNOS, underscoring the importance of these enzymes in the pathophysiology and maintenance of genetic hypertension. |
| 712 | 12797599 | In kidney, nitric oxide (NO) synthesized by nitric oxide synthase (NOS) regulates sodium and water excretion, and renal medullary blood flow. |
| 713 | 12797599 | The expression of constitutive NOS, endothelial NOS (eNOS) and neuronal NOS (nNOS), were assessed in kidney of the spontaneously hypertensive rat (SHR) and the normotensive Wistar Kyoto (WKY) rat by Western blot analysis and immunocytochemistry. |
| 714 | 12797599 | Neuronal NOS expression was observed in the cortex and eNOS was detected only in theinner medulla of both WKY and SHR. |
| 715 | 12797599 | In SHR, expression of eNOS was attenuated to 35.1 +/- 10.8%, while expression of nNOS was only 57.5 +/- 5.7% of the levels seen in WKY rat. |
| 716 | 12797599 | The decreased renal blood flow observed in SHR may be linked to a diminished expression of eNOS and nNOS, underscoring the importance of these enzymes in the pathophysiology and maintenance of genetic hypertension. |
| 717 | 12797599 | In kidney, nitric oxide (NO) synthesized by nitric oxide synthase (NOS) regulates sodium and water excretion, and renal medullary blood flow. |
| 718 | 12797599 | The expression of constitutive NOS, endothelial NOS (eNOS) and neuronal NOS (nNOS), were assessed in kidney of the spontaneously hypertensive rat (SHR) and the normotensive Wistar Kyoto (WKY) rat by Western blot analysis and immunocytochemistry. |
| 719 | 12797599 | Neuronal NOS expression was observed in the cortex and eNOS was detected only in theinner medulla of both WKY and SHR. |
| 720 | 12797599 | In SHR, expression of eNOS was attenuated to 35.1 +/- 10.8%, while expression of nNOS was only 57.5 +/- 5.7% of the levels seen in WKY rat. |
| 721 | 12797599 | The decreased renal blood flow observed in SHR may be linked to a diminished expression of eNOS and nNOS, underscoring the importance of these enzymes in the pathophysiology and maintenance of genetic hypertension. |
| 722 | 12811832 | However, diabetes induced modifications in phenotype and nitric oxide synthase(s) (NOS) expression and activity in vSMC have not been fully characterized. |
| 723 | 12811832 | In the same cells, as compared to CR cells, eNOS mRNA levels and NOS activity were increased, while intracellular cGMP level was lower and superoxide anion production was significantly greater. |
| 724 | 12811832 | However, diabetes induced modifications in phenotype and nitric oxide synthase(s) (NOS) expression and activity in vSMC have not been fully characterized. |
| 725 | 12811832 | In the same cells, as compared to CR cells, eNOS mRNA levels and NOS activity were increased, while intracellular cGMP level was lower and superoxide anion production was significantly greater. |
| 726 | 12856869 | In the present study, the effect of acupuncture at Zusanli acupoint on nitric oxide synthase (NOS) expression in the hippocampus of streptozotocin (STZ)-induced diabetic rats was investigated via nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry. |
| 727 | 12857060 | The effects of nitric oxide synthase (NOS) inhibition by Nw-nitro-L-arginine methyl ester (L-NAME) administration on oxidative stress parameters were investigated in streptozotocin (STZ) induced diabetic rats. |
| 728 | 12860450 | The effect of nitric oxide synthase (NOS) inhibition on acetylcholine-induced vasodilator response was investigated. |
| 729 | 12879114 | Therapeutic stimulation of penile nitric oxide synthase (NOS) and related pathways. |
| 730 | 12889622 | Diabetes and nitric oxide synthase (NOS) inhibition both exacerbate mesenteric ischemia/ reperfusion injury. |
| 731 | 12889622 | The aim of this study was to determine the effects of diabetes and NOS inhibition on HSP-72 induction in vivo. |
| 732 | 12889622 | NOS is required for HSP-72 expression, but not survival. |
| 733 | 12889622 | Diabetes and nitric oxide synthase (NOS) inhibition both exacerbate mesenteric ischemia/ reperfusion injury. |
| 734 | 12889622 | The aim of this study was to determine the effects of diabetes and NOS inhibition on HSP-72 induction in vivo. |
| 735 | 12889622 | NOS is required for HSP-72 expression, but not survival. |
| 736 | 12889622 | Diabetes and nitric oxide synthase (NOS) inhibition both exacerbate mesenteric ischemia/ reperfusion injury. |
| 737 | 12889622 | The aim of this study was to determine the effects of diabetes and NOS inhibition on HSP-72 induction in vivo. |
| 738 | 12889622 | NOS is required for HSP-72 expression, but not survival. |
| 739 | 12934955 | Effect of acupuncture on the expressions of nitric oxide synthase (NOS) and neuronal NOS (nNOS) in the cerebral cortex of streptozotocin (STZ)-induced diabetic rats was investigated. |
| 740 | 12934955 | From the results, acupuncture was shown to increase the numbers of nicotinamide adenine dinucleotide phosphate-diaphorase-positive and nNOS-positive neurons in STZ-induced diabetic rats. |
| 741 | 12934955 | Effect of acupuncture on the expressions of nitric oxide synthase (NOS) and neuronal NOS (nNOS) in the cerebral cortex of streptozotocin (STZ)-induced diabetic rats was investigated. |
| 742 | 12934955 | From the results, acupuncture was shown to increase the numbers of nicotinamide adenine dinucleotide phosphate-diaphorase-positive and nNOS-positive neurons in STZ-induced diabetic rats. |
| 743 | 14506635 | Using immunohistochemical techniques, we assessed the vascular density and distribution of angiogenesis (FVIII) and vascular endothelial growth factor (VEGF) expression as well as the expression of 2 VEGF receptors, Flt-1 and Flk-1, in 55 nonrheumatic and 6 control aortic valves. |
| 744 | 14506635 | In the light of the fact that the angiogenic effect of VEGF is mediated by sustained formation of nitric oxide, the samples were also immunostained with 3 nitric oxide synthase (eNOS, iNOS, and nNOS) antibodies. |
| 745 | 14506635 | Diseased valves showed distinct VEGF, Flt-1, Flk-1, and eNOS positivity of activated endothelial, stromal fusiform myofibroblastic, and histocytic cells. |
| 746 | 14506635 | In contrast, immunoreactivity for iNOS and nNOS was seen only in nonendothelial stromal cells, and their expression was weaker. |
| 747 | 14506635 | Using immunohistochemical techniques, we assessed the vascular density and distribution of angiogenesis (FVIII) and vascular endothelial growth factor (VEGF) expression as well as the expression of 2 VEGF receptors, Flt-1 and Flk-1, in 55 nonrheumatic and 6 control aortic valves. |
| 748 | 14506635 | In the light of the fact that the angiogenic effect of VEGF is mediated by sustained formation of nitric oxide, the samples were also immunostained with 3 nitric oxide synthase (eNOS, iNOS, and nNOS) antibodies. |
| 749 | 14506635 | Diseased valves showed distinct VEGF, Flt-1, Flk-1, and eNOS positivity of activated endothelial, stromal fusiform myofibroblastic, and histocytic cells. |
| 750 | 14506635 | In contrast, immunoreactivity for iNOS and nNOS was seen only in nonendothelial stromal cells, and their expression was weaker. |
| 751 | 14562136 | Penile tissue was harvested to determine the changes in tissue morphology including neuronal nitric oxide synthase, smooth muscle alpha-actin and endothelial cell integrity. |
| 752 | 14643905 | Moreover, nitric oxide synthase (NOS) activity of aortic endothelial cells was assessed in both diabetic and healthy rats using histochemical staining for nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase activity. |
| 753 | 14654370 | Frozen tissues were subjected to HO-1 and HO-2 mRNA expression by real-time RT-PCR and HO activity determination. |
| 754 | 14654370 | Paraffin-embedded tissue sections were used for immunohistochemical analysis of HO-1 and HO-2. 8-Hydroxy-2'-deoxyguanosine (8-OHdG) stain, a sensitive and specific marker of DNA damage, was preformed to assess damage induced by oxidative stress. |
| 755 | 14654370 | A possible relationship between the HO and the nitric oxide (NO) pathways was also considered by studying the mRNA levels of endothelial nitric oxide synthase (NOS) and inducible NOS, and by measuring the amount of NOS products. |
| 756 | 14690489 | Western blots demonstrated that there was no inducible-nitric oxide synthase (iNOS) in control or diabetic tissues and that the levels of endothelial-NOS (eNOS) and neuronal-NOS (nNOS) detected were not statistically significantly different. |
| 757 | 14706871 | Among other factors, penile erection is induced by activation of nitric oxide synthase (NOS). |
| 758 | 14706871 | NOS-containing neurons are identical to the populations of neurons selectively stained for NADPH-diaphorase activity. |
| 759 | 14706871 | Using this technique, we have evaluated changes of NOS in the lumbar spinal cord of diabetic rats with or without insulin treatment. |
| 760 | 14706871 | Among other factors, penile erection is induced by activation of nitric oxide synthase (NOS). |
| 761 | 14706871 | NOS-containing neurons are identical to the populations of neurons selectively stained for NADPH-diaphorase activity. |
| 762 | 14706871 | Using this technique, we have evaluated changes of NOS in the lumbar spinal cord of diabetic rats with or without insulin treatment. |
| 763 | 14706871 | Among other factors, penile erection is induced by activation of nitric oxide synthase (NOS). |
| 764 | 14706871 | NOS-containing neurons are identical to the populations of neurons selectively stained for NADPH-diaphorase activity. |
| 765 | 14706871 | Using this technique, we have evaluated changes of NOS in the lumbar spinal cord of diabetic rats with or without insulin treatment. |
| 766 | 14729730 | Our goal was to examine whether exercise training alleviates impaired nitric oxide synthase (NOS)-dependent dilatation of the basilar artery in Type 1 diabetic rats. |
| 767 | 14729730 | Finally, we found that endothelial NOS (eNOS) protein in the basilar artery was higher in diabetic compared with nondiabetic rats and that exercise increased eNOS protein in the basilar artery of nondiabetic and diabetic rats. |
| 768 | 14729730 | We conclude that 1) exercise can alleviate impaired NOS-dependent dilatation of the basilar artery during diabetes mellitus, 2) the synthesis and release of nitric oxide accounts for dilatation of the basilar artery to acetylcholine in sedentary and exercised nondiabetic and diabetic rats, and 3) exercise may exert its affect on cerebrovascular reactivity during diabetes by altering levels of eNOS protein in the basilar artery. |
| 769 | 14729730 | Our goal was to examine whether exercise training alleviates impaired nitric oxide synthase (NOS)-dependent dilatation of the basilar artery in Type 1 diabetic rats. |
| 770 | 14729730 | Finally, we found that endothelial NOS (eNOS) protein in the basilar artery was higher in diabetic compared with nondiabetic rats and that exercise increased eNOS protein in the basilar artery of nondiabetic and diabetic rats. |
| 771 | 14729730 | We conclude that 1) exercise can alleviate impaired NOS-dependent dilatation of the basilar artery during diabetes mellitus, 2) the synthesis and release of nitric oxide accounts for dilatation of the basilar artery to acetylcholine in sedentary and exercised nondiabetic and diabetic rats, and 3) exercise may exert its affect on cerebrovascular reactivity during diabetes by altering levels of eNOS protein in the basilar artery. |
| 772 | 14729730 | Our goal was to examine whether exercise training alleviates impaired nitric oxide synthase (NOS)-dependent dilatation of the basilar artery in Type 1 diabetic rats. |
| 773 | 14729730 | Finally, we found that endothelial NOS (eNOS) protein in the basilar artery was higher in diabetic compared with nondiabetic rats and that exercise increased eNOS protein in the basilar artery of nondiabetic and diabetic rats. |
| 774 | 14729730 | We conclude that 1) exercise can alleviate impaired NOS-dependent dilatation of the basilar artery during diabetes mellitus, 2) the synthesis and release of nitric oxide accounts for dilatation of the basilar artery to acetylcholine in sedentary and exercised nondiabetic and diabetic rats, and 3) exercise may exert its affect on cerebrovascular reactivity during diabetes by altering levels of eNOS protein in the basilar artery. |
| 775 | 14961189 | Despite the compensatory increase in expression of iNOS and nNOS, nitric oxide bioavailability is reduced because of increased reaction rates with superoxide, yielding as by-products reactive nitrogen/oxygen species that induce protein nitration. |
| 776 | 14963467 | Erectile dysfunction associated with diabetes mellitus is caused in part by disordered endothelial smooth muscle relaxation, neuropathy, and a decrease in cavernosal nitric oxide synthase (NOS) activity. |
| 777 | 14963467 | The purpose of this study was to determine whether a combination of sildenafil and adenoviral gene transfer of endothelial NOS (eNOS) could enhance the erectile response in diabetic rats. |
| 778 | 14963467 | Erectile dysfunction associated with diabetes mellitus is caused in part by disordered endothelial smooth muscle relaxation, neuropathy, and a decrease in cavernosal nitric oxide synthase (NOS) activity. |
| 779 | 14963467 | The purpose of this study was to determine whether a combination of sildenafil and adenoviral gene transfer of endothelial NOS (eNOS) could enhance the erectile response in diabetic rats. |
| 780 | 15010356 | Inhibition of nNOS expression in the macula densa by COX-2-derived prostaglandin E(2). |
| 781 | 15010356 | It is well established that cyclooxygenase-2 (COX-2) and the neuronal form of nitric oxide synthase (nNOS) are coexpressed in macula densa cells and that the expression of both enzymes is stimulated in a number of high-renin states. |
| 782 | 15010356 | To further explore the role of nNOS and COX-2 in renin secretion, we determined plasma renin activity in mice deficient in nNOS or COX-2. |
| 783 | 15010356 | Plasma renin activity was significantly reduced in nNOS -/- mice on a mixed genetic background and in COX-2 -/- mice on either BALB/c or C57/BL6 congenic backgrounds. |
| 784 | 15010356 | In COX-2 -/- mice, nNOS mRNA expression in the kidney, determined by real-time RT-PCR, was upregulated throughout the postnatal periods, ranging from postnatal day (PND) 3 to PND 60. |
| 785 | 15010356 | The induction of nNOS protein expression and NOS activity in COX-2 -/- mice was localized to macula densa cells using immunohistochemistry and NADPH-diaphorase staining methods, respectively. |
| 786 | 15010356 | Therefore, these findings reveal that the absence of either COX-2 or nNOS is associated with suppressed renin secretion. |
| 787 | 15010356 | Furthermore, the inhibitory effect of PGE(2) on nNOS mRNA expression indicates a novel interaction between NO and prostaglandin-mediated pathways of renin regulation. |
| 788 | 15010356 | Inhibition of nNOS expression in the macula densa by COX-2-derived prostaglandin E(2). |
| 789 | 15010356 | It is well established that cyclooxygenase-2 (COX-2) and the neuronal form of nitric oxide synthase (nNOS) are coexpressed in macula densa cells and that the expression of both enzymes is stimulated in a number of high-renin states. |
| 790 | 15010356 | To further explore the role of nNOS and COX-2 in renin secretion, we determined plasma renin activity in mice deficient in nNOS or COX-2. |
| 791 | 15010356 | Plasma renin activity was significantly reduced in nNOS -/- mice on a mixed genetic background and in COX-2 -/- mice on either BALB/c or C57/BL6 congenic backgrounds. |
| 792 | 15010356 | In COX-2 -/- mice, nNOS mRNA expression in the kidney, determined by real-time RT-PCR, was upregulated throughout the postnatal periods, ranging from postnatal day (PND) 3 to PND 60. |
| 793 | 15010356 | The induction of nNOS protein expression and NOS activity in COX-2 -/- mice was localized to macula densa cells using immunohistochemistry and NADPH-diaphorase staining methods, respectively. |
| 794 | 15010356 | Therefore, these findings reveal that the absence of either COX-2 or nNOS is associated with suppressed renin secretion. |
| 795 | 15010356 | Furthermore, the inhibitory effect of PGE(2) on nNOS mRNA expression indicates a novel interaction between NO and prostaglandin-mediated pathways of renin regulation. |
| 796 | 15010356 | Inhibition of nNOS expression in the macula densa by COX-2-derived prostaglandin E(2). |
| 797 | 15010356 | It is well established that cyclooxygenase-2 (COX-2) and the neuronal form of nitric oxide synthase (nNOS) are coexpressed in macula densa cells and that the expression of both enzymes is stimulated in a number of high-renin states. |
| 798 | 15010356 | To further explore the role of nNOS and COX-2 in renin secretion, we determined plasma renin activity in mice deficient in nNOS or COX-2. |
| 799 | 15010356 | Plasma renin activity was significantly reduced in nNOS -/- mice on a mixed genetic background and in COX-2 -/- mice on either BALB/c or C57/BL6 congenic backgrounds. |
| 800 | 15010356 | In COX-2 -/- mice, nNOS mRNA expression in the kidney, determined by real-time RT-PCR, was upregulated throughout the postnatal periods, ranging from postnatal day (PND) 3 to PND 60. |
| 801 | 15010356 | The induction of nNOS protein expression and NOS activity in COX-2 -/- mice was localized to macula densa cells using immunohistochemistry and NADPH-diaphorase staining methods, respectively. |
| 802 | 15010356 | Therefore, these findings reveal that the absence of either COX-2 or nNOS is associated with suppressed renin secretion. |
| 803 | 15010356 | Furthermore, the inhibitory effect of PGE(2) on nNOS mRNA expression indicates a novel interaction between NO and prostaglandin-mediated pathways of renin regulation. |
| 804 | 15010356 | Inhibition of nNOS expression in the macula densa by COX-2-derived prostaglandin E(2). |
| 805 | 15010356 | It is well established that cyclooxygenase-2 (COX-2) and the neuronal form of nitric oxide synthase (nNOS) are coexpressed in macula densa cells and that the expression of both enzymes is stimulated in a number of high-renin states. |
| 806 | 15010356 | To further explore the role of nNOS and COX-2 in renin secretion, we determined plasma renin activity in mice deficient in nNOS or COX-2. |
| 807 | 15010356 | Plasma renin activity was significantly reduced in nNOS -/- mice on a mixed genetic background and in COX-2 -/- mice on either BALB/c or C57/BL6 congenic backgrounds. |
| 808 | 15010356 | In COX-2 -/- mice, nNOS mRNA expression in the kidney, determined by real-time RT-PCR, was upregulated throughout the postnatal periods, ranging from postnatal day (PND) 3 to PND 60. |
| 809 | 15010356 | The induction of nNOS protein expression and NOS activity in COX-2 -/- mice was localized to macula densa cells using immunohistochemistry and NADPH-diaphorase staining methods, respectively. |
| 810 | 15010356 | Therefore, these findings reveal that the absence of either COX-2 or nNOS is associated with suppressed renin secretion. |
| 811 | 15010356 | Furthermore, the inhibitory effect of PGE(2) on nNOS mRNA expression indicates a novel interaction between NO and prostaglandin-mediated pathways of renin regulation. |
| 812 | 15010356 | Inhibition of nNOS expression in the macula densa by COX-2-derived prostaglandin E(2). |
| 813 | 15010356 | It is well established that cyclooxygenase-2 (COX-2) and the neuronal form of nitric oxide synthase (nNOS) are coexpressed in macula densa cells and that the expression of both enzymes is stimulated in a number of high-renin states. |
| 814 | 15010356 | To further explore the role of nNOS and COX-2 in renin secretion, we determined plasma renin activity in mice deficient in nNOS or COX-2. |
| 815 | 15010356 | Plasma renin activity was significantly reduced in nNOS -/- mice on a mixed genetic background and in COX-2 -/- mice on either BALB/c or C57/BL6 congenic backgrounds. |
| 816 | 15010356 | In COX-2 -/- mice, nNOS mRNA expression in the kidney, determined by real-time RT-PCR, was upregulated throughout the postnatal periods, ranging from postnatal day (PND) 3 to PND 60. |
| 817 | 15010356 | The induction of nNOS protein expression and NOS activity in COX-2 -/- mice was localized to macula densa cells using immunohistochemistry and NADPH-diaphorase staining methods, respectively. |
| 818 | 15010356 | Therefore, these findings reveal that the absence of either COX-2 or nNOS is associated with suppressed renin secretion. |
| 819 | 15010356 | Furthermore, the inhibitory effect of PGE(2) on nNOS mRNA expression indicates a novel interaction between NO and prostaglandin-mediated pathways of renin regulation. |
| 820 | 15010356 | Inhibition of nNOS expression in the macula densa by COX-2-derived prostaglandin E(2). |
| 821 | 15010356 | It is well established that cyclooxygenase-2 (COX-2) and the neuronal form of nitric oxide synthase (nNOS) are coexpressed in macula densa cells and that the expression of both enzymes is stimulated in a number of high-renin states. |
| 822 | 15010356 | To further explore the role of nNOS and COX-2 in renin secretion, we determined plasma renin activity in mice deficient in nNOS or COX-2. |
| 823 | 15010356 | Plasma renin activity was significantly reduced in nNOS -/- mice on a mixed genetic background and in COX-2 -/- mice on either BALB/c or C57/BL6 congenic backgrounds. |
| 824 | 15010356 | In COX-2 -/- mice, nNOS mRNA expression in the kidney, determined by real-time RT-PCR, was upregulated throughout the postnatal periods, ranging from postnatal day (PND) 3 to PND 60. |
| 825 | 15010356 | The induction of nNOS protein expression and NOS activity in COX-2 -/- mice was localized to macula densa cells using immunohistochemistry and NADPH-diaphorase staining methods, respectively. |
| 826 | 15010356 | Therefore, these findings reveal that the absence of either COX-2 or nNOS is associated with suppressed renin secretion. |
| 827 | 15010356 | Furthermore, the inhibitory effect of PGE(2) on nNOS mRNA expression indicates a novel interaction between NO and prostaglandin-mediated pathways of renin regulation. |
| 828 | 15010356 | Inhibition of nNOS expression in the macula densa by COX-2-derived prostaglandin E(2). |
| 829 | 15010356 | It is well established that cyclooxygenase-2 (COX-2) and the neuronal form of nitric oxide synthase (nNOS) are coexpressed in macula densa cells and that the expression of both enzymes is stimulated in a number of high-renin states. |
| 830 | 15010356 | To further explore the role of nNOS and COX-2 in renin secretion, we determined plasma renin activity in mice deficient in nNOS or COX-2. |
| 831 | 15010356 | Plasma renin activity was significantly reduced in nNOS -/- mice on a mixed genetic background and in COX-2 -/- mice on either BALB/c or C57/BL6 congenic backgrounds. |
| 832 | 15010356 | In COX-2 -/- mice, nNOS mRNA expression in the kidney, determined by real-time RT-PCR, was upregulated throughout the postnatal periods, ranging from postnatal day (PND) 3 to PND 60. |
| 833 | 15010356 | The induction of nNOS protein expression and NOS activity in COX-2 -/- mice was localized to macula densa cells using immunohistochemistry and NADPH-diaphorase staining methods, respectively. |
| 834 | 15010356 | Therefore, these findings reveal that the absence of either COX-2 or nNOS is associated with suppressed renin secretion. |
| 835 | 15010356 | Furthermore, the inhibitory effect of PGE(2) on nNOS mRNA expression indicates a novel interaction between NO and prostaglandin-mediated pathways of renin regulation. |
| 836 | 15010356 | Inhibition of nNOS expression in the macula densa by COX-2-derived prostaglandin E(2). |
| 837 | 15010356 | It is well established that cyclooxygenase-2 (COX-2) and the neuronal form of nitric oxide synthase (nNOS) are coexpressed in macula densa cells and that the expression of both enzymes is stimulated in a number of high-renin states. |
| 838 | 15010356 | To further explore the role of nNOS and COX-2 in renin secretion, we determined plasma renin activity in mice deficient in nNOS or COX-2. |
| 839 | 15010356 | Plasma renin activity was significantly reduced in nNOS -/- mice on a mixed genetic background and in COX-2 -/- mice on either BALB/c or C57/BL6 congenic backgrounds. |
| 840 | 15010356 | In COX-2 -/- mice, nNOS mRNA expression in the kidney, determined by real-time RT-PCR, was upregulated throughout the postnatal periods, ranging from postnatal day (PND) 3 to PND 60. |
| 841 | 15010356 | The induction of nNOS protein expression and NOS activity in COX-2 -/- mice was localized to macula densa cells using immunohistochemistry and NADPH-diaphorase staining methods, respectively. |
| 842 | 15010356 | Therefore, these findings reveal that the absence of either COX-2 or nNOS is associated with suppressed renin secretion. |
| 843 | 15010356 | Furthermore, the inhibitory effect of PGE(2) on nNOS mRNA expression indicates a novel interaction between NO and prostaglandin-mediated pathways of renin regulation. |
| 844 | 15048017 | We have shown that the administration of tetrahydrobiopterin, an important co-factor for nitric oxide synthase (NOS) partially restores endothelial function (1) in leptin-deficient mice (db/db) with spontaneous type II diabetes, as well as (2) in human vascular tissue harvested for coronary artery bypass grafting (CABG). |
| 845 | 15050532 | Stimulatory effect of IGF-I and VEGF on eNOS message, protein expression, eNOS phosphorylation and nitric oxide production in rat glomeruli, and the involvement of PI3-K signaling pathway. |
| 846 | 15050532 | We set out to determine whether IGF-I and/or VEGF165 directly stimulate NO production in rat glomeruli and whether the expression of NO synthase (NOS) isoforms as well as eNOS phosphorylation contribute to NO generation by IGF-I and VEGF. |
| 847 | 15050532 | Long-term exposure to IGF-I and/or VEGF165 augments NO production through increased eNOS mRNA, protein expression and phosphatidylinositol 3-kinase (PI3-K) signaling pathway plays a major role in this process; short-term exposure to IGF-I and/or VEGF(165) activates eNOS activity via phosphorylation by a PI3-K/Akt dependent pathway. |
| 848 | 15050532 | Our data suggest the great possibility that increased endogenous IGF-I and VEGF may be responsible for the up-regulation of eNOS expression and NO production which contributes to glomerular hyperfiltration in early diabetic kidneys. |
| 849 | 15050532 | IGF-I is a newly described growth factor that up-regulates eNOS expression and PI3-K plays a major role in this process. |
| 850 | 15075180 | Experiments were performed in neuronal (nNOS)- and endothelial nitric oxide synthase (eNOS)-deficient mice to study the role of nitric oxide (NO) in macula densa control of renin secretion in vivo and in the isolated, perfused mouse kidney. |
| 851 | 15075180 | Increases in plasma renin concentration (PRC) in response to a 3-day infusion of bumetanide (50 mg.kg(-1).day(-1)) or an acute injection of furosemide (50 mg/kg ip) were not markedly altered in nNOS-/- mice. |
| 852 | 15075180 | In the isolated kidney preparation, bumetanide caused similar relative increases in renin secretion in kidneys of wild-type, nNOS-/-, and eNOS-/- mice. |
| 853 | 15075180 | Basal PRC was significantly reduced in male nNOS-/- mice compared with nNOS+/+ (189 +/- 28 vs. 355 +/- 57 ng ANG I.ml(-1).h(-1); P = 0.017). |
| 854 | 15075180 | There was no significant difference in PRC between eNOS+/+ and eNOS-/- mice. |
| 855 | 15075180 | Basal renin secretion rates in perfused kidneys isolated from nNOS-/- or eNOS-/- mice were markedly reduced compared with wild-type controls. |
| 856 | 15075180 | Our data suggest that NO generated by macula densa nNOS does not play a specific mediator role in macula densa-dependent renin secretion. |
| 857 | 15075180 | Experiments were performed in neuronal (nNOS)- and endothelial nitric oxide synthase (eNOS)-deficient mice to study the role of nitric oxide (NO) in macula densa control of renin secretion in vivo and in the isolated, perfused mouse kidney. |
| 858 | 15075180 | Increases in plasma renin concentration (PRC) in response to a 3-day infusion of bumetanide (50 mg.kg(-1).day(-1)) or an acute injection of furosemide (50 mg/kg ip) were not markedly altered in nNOS-/- mice. |
| 859 | 15075180 | In the isolated kidney preparation, bumetanide caused similar relative increases in renin secretion in kidneys of wild-type, nNOS-/-, and eNOS-/- mice. |
| 860 | 15075180 | Basal PRC was significantly reduced in male nNOS-/- mice compared with nNOS+/+ (189 +/- 28 vs. 355 +/- 57 ng ANG I.ml(-1).h(-1); P = 0.017). |
| 861 | 15075180 | There was no significant difference in PRC between eNOS+/+ and eNOS-/- mice. |
| 862 | 15075180 | Basal renin secretion rates in perfused kidneys isolated from nNOS-/- or eNOS-/- mice were markedly reduced compared with wild-type controls. |
| 863 | 15075180 | Our data suggest that NO generated by macula densa nNOS does not play a specific mediator role in macula densa-dependent renin secretion. |
| 864 | 15075180 | Experiments were performed in neuronal (nNOS)- and endothelial nitric oxide synthase (eNOS)-deficient mice to study the role of nitric oxide (NO) in macula densa control of renin secretion in vivo and in the isolated, perfused mouse kidney. |
| 865 | 15075180 | Increases in plasma renin concentration (PRC) in response to a 3-day infusion of bumetanide (50 mg.kg(-1).day(-1)) or an acute injection of furosemide (50 mg/kg ip) were not markedly altered in nNOS-/- mice. |
| 866 | 15075180 | In the isolated kidney preparation, bumetanide caused similar relative increases in renin secretion in kidneys of wild-type, nNOS-/-, and eNOS-/- mice. |
| 867 | 15075180 | Basal PRC was significantly reduced in male nNOS-/- mice compared with nNOS+/+ (189 +/- 28 vs. 355 +/- 57 ng ANG I.ml(-1).h(-1); P = 0.017). |
| 868 | 15075180 | There was no significant difference in PRC between eNOS+/+ and eNOS-/- mice. |
| 869 | 15075180 | Basal renin secretion rates in perfused kidneys isolated from nNOS-/- or eNOS-/- mice were markedly reduced compared with wild-type controls. |
| 870 | 15075180 | Our data suggest that NO generated by macula densa nNOS does not play a specific mediator role in macula densa-dependent renin secretion. |
| 871 | 15075180 | Experiments were performed in neuronal (nNOS)- and endothelial nitric oxide synthase (eNOS)-deficient mice to study the role of nitric oxide (NO) in macula densa control of renin secretion in vivo and in the isolated, perfused mouse kidney. |
| 872 | 15075180 | Increases in plasma renin concentration (PRC) in response to a 3-day infusion of bumetanide (50 mg.kg(-1).day(-1)) or an acute injection of furosemide (50 mg/kg ip) were not markedly altered in nNOS-/- mice. |
| 873 | 15075180 | In the isolated kidney preparation, bumetanide caused similar relative increases in renin secretion in kidneys of wild-type, nNOS-/-, and eNOS-/- mice. |
| 874 | 15075180 | Basal PRC was significantly reduced in male nNOS-/- mice compared with nNOS+/+ (189 +/- 28 vs. 355 +/- 57 ng ANG I.ml(-1).h(-1); P = 0.017). |
| 875 | 15075180 | There was no significant difference in PRC between eNOS+/+ and eNOS-/- mice. |
| 876 | 15075180 | Basal renin secretion rates in perfused kidneys isolated from nNOS-/- or eNOS-/- mice were markedly reduced compared with wild-type controls. |
| 877 | 15075180 | Our data suggest that NO generated by macula densa nNOS does not play a specific mediator role in macula densa-dependent renin secretion. |
| 878 | 15127883 | In the corpus cavernosum of SHR, expression of the HO-2 and nNOS genes was similar, and NOx levels after EFS were similar to those of WKY. cGMP levels after EFS and the relaxation evoked by the NO donor was lower in SHR than WKY. |
| 879 | 15149729 | We have also established that the neuronal isoform of constitutive NO synthase (nNOS) is expressed in beta-cells and modulates insulin secretion. |
| 880 | 15149729 | In this study, we explored the kinetics of glucose- and arginine-stimulated insulin release in perifused isolated islets as well as the effect of N-omega-nitro-L-arginine methyl ester (L-NAME), a NOS inhibitor, to get insight into the possible mechanisms responsible for the arginine hypersensitivity observed in vitro in this and other models of type 2 diabetes. |
| 881 | 15149729 | The addition of L-NAME to control islets markedly enhanced the insulin response to arginine, as expected from the documented inhibitory effect exerted by nNOS activity in normal beta-cells, whereas it did not further modify the insulin secretion in diabetic islets, thus implying the occurrence of a defective nNOS activity in these islets. |
| 882 | 15149729 | In conclusion, our results provide for the first time evidence that functional abnormalities of type 2 experimental diabetes, such as the insulin hyper-responsiveness to arginine, could be due to an impairment of nNOS expression and/or activity in beta-cells. |
| 883 | 15149729 | We have also established that the neuronal isoform of constitutive NO synthase (nNOS) is expressed in beta-cells and modulates insulin secretion. |
| 884 | 15149729 | In this study, we explored the kinetics of glucose- and arginine-stimulated insulin release in perifused isolated islets as well as the effect of N-omega-nitro-L-arginine methyl ester (L-NAME), a NOS inhibitor, to get insight into the possible mechanisms responsible for the arginine hypersensitivity observed in vitro in this and other models of type 2 diabetes. |
| 885 | 15149729 | The addition of L-NAME to control islets markedly enhanced the insulin response to arginine, as expected from the documented inhibitory effect exerted by nNOS activity in normal beta-cells, whereas it did not further modify the insulin secretion in diabetic islets, thus implying the occurrence of a defective nNOS activity in these islets. |
| 886 | 15149729 | In conclusion, our results provide for the first time evidence that functional abnormalities of type 2 experimental diabetes, such as the insulin hyper-responsiveness to arginine, could be due to an impairment of nNOS expression and/or activity in beta-cells. |
| 887 | 15149729 | We have also established that the neuronal isoform of constitutive NO synthase (nNOS) is expressed in beta-cells and modulates insulin secretion. |
| 888 | 15149729 | In this study, we explored the kinetics of glucose- and arginine-stimulated insulin release in perifused isolated islets as well as the effect of N-omega-nitro-L-arginine methyl ester (L-NAME), a NOS inhibitor, to get insight into the possible mechanisms responsible for the arginine hypersensitivity observed in vitro in this and other models of type 2 diabetes. |
| 889 | 15149729 | The addition of L-NAME to control islets markedly enhanced the insulin response to arginine, as expected from the documented inhibitory effect exerted by nNOS activity in normal beta-cells, whereas it did not further modify the insulin secretion in diabetic islets, thus implying the occurrence of a defective nNOS activity in these islets. |
| 890 | 15149729 | In conclusion, our results provide for the first time evidence that functional abnormalities of type 2 experimental diabetes, such as the insulin hyper-responsiveness to arginine, could be due to an impairment of nNOS expression and/or activity in beta-cells. |
| 891 | 15149729 | We have also established that the neuronal isoform of constitutive NO synthase (nNOS) is expressed in beta-cells and modulates insulin secretion. |
| 892 | 15149729 | In this study, we explored the kinetics of glucose- and arginine-stimulated insulin release in perifused isolated islets as well as the effect of N-omega-nitro-L-arginine methyl ester (L-NAME), a NOS inhibitor, to get insight into the possible mechanisms responsible for the arginine hypersensitivity observed in vitro in this and other models of type 2 diabetes. |
| 893 | 15149729 | The addition of L-NAME to control islets markedly enhanced the insulin response to arginine, as expected from the documented inhibitory effect exerted by nNOS activity in normal beta-cells, whereas it did not further modify the insulin secretion in diabetic islets, thus implying the occurrence of a defective nNOS activity in these islets. |
| 894 | 15149729 | In conclusion, our results provide for the first time evidence that functional abnormalities of type 2 experimental diabetes, such as the insulin hyper-responsiveness to arginine, could be due to an impairment of nNOS expression and/or activity in beta-cells. |
| 895 | 15161750 | Changes in the dimeric state of neuronal nitric oxide synthase affect the kinetics of secretagogue-induced insulin response. |
| 896 | 15161750 | We previously showed that pancreatic beta-cells express a neuronal isoform of nitric oxide synthase (nNOS) that controls insulin secretion by exerting two enzymatic activities: nitric oxide (NO) production and cytochrome c reductase activity. |
| 897 | 15161750 | We now bring evidence that two inhibitors of nNOS, N-omega-nitro-l-arginine methyl ester (l-NAME) and 7-nitroindazole (7-NI), increase glucose-induced insulin secretion but affect beta-cell function differently. |
| 898 | 15161750 | Changes in the dimeric state of neuronal nitric oxide synthase affect the kinetics of secretagogue-induced insulin response. |
| 899 | 15161750 | We previously showed that pancreatic beta-cells express a neuronal isoform of nitric oxide synthase (nNOS) that controls insulin secretion by exerting two enzymatic activities: nitric oxide (NO) production and cytochrome c reductase activity. |
| 900 | 15161750 | We now bring evidence that two inhibitors of nNOS, N-omega-nitro-l-arginine methyl ester (l-NAME) and 7-nitroindazole (7-NI), increase glucose-induced insulin secretion but affect beta-cell function differently. |
| 901 | 15161750 | Changes in the dimeric state of neuronal nitric oxide synthase affect the kinetics of secretagogue-induced insulin response. |
| 902 | 15161750 | We previously showed that pancreatic beta-cells express a neuronal isoform of nitric oxide synthase (nNOS) that controls insulin secretion by exerting two enzymatic activities: nitric oxide (NO) production and cytochrome c reductase activity. |
| 903 | 15161750 | We now bring evidence that two inhibitors of nNOS, N-omega-nitro-l-arginine methyl ester (l-NAME) and 7-nitroindazole (7-NI), increase glucose-induced insulin secretion but affect beta-cell function differently. |
| 904 | 15184671 | RhoA/Rho-kinase suppresses endothelial nitric oxide synthase in the penis: a mechanism for diabetes-associated erectile dysfunction. |
| 905 | 15184671 | RhoA/Rho-kinase may suppress endothelial nitric oxide synthase (eNOS). |
| 906 | 15184671 | Here, we tested the hypothesis that RhoA/Rho-kinase contributes to diabetes-related erectile dysfunction and down-regulation of eNOS in the streptozotocin (STZ)-diabetic rat penis. |
| 907 | 15184671 | Colocalization of Rho-kinase and eNOS protein was present in the endothelium of the corpus cavernosum. |
| 908 | 15184671 | RhoA/Rho-kinase protein abundance and MYPT-1 phosphorylation at Thr-696 were elevated in the STZ-diabetic rat penis. |
| 909 | 15184671 | In addition, eNOS protein expression, cavernosal constitutive NOS activity, and cGMP levels were reduced in the STZ-diabetic penis. |
| 910 | 15184671 | To assess the functional role of RhoA/Rho-kinase in the penis, we evaluated the effects of an adeno-associated virus encoding the dominant-negative RhoA mutant (AAVTCMV19NRhoA) on RhoA/Rho-kinase and eNOS and erectile function in vivo in the STZ-diabetic rat. |
| 911 | 15184671 | STZ-diabetic rats transfected with AAVCMVT19NRhoA had a reduction in RhoA/Rho-kinase and MYPT-1 phosphorylation at a time when cavernosal eNOS protein, constitutive NOS activity, and cGMP levels were restored to levels found in the control rats. |
| 912 | 15184671 | These data demonstrate a previously undescribed mechanism for the down-regulation of penile eNOS in diabetes mediated by activation of the RhoA/Rho-kinase pathway. |
| 913 | 15184671 | Importantly, these data imply that inhibition of RhoA/Rho-kinase improves eNOS protein content and activity thus restoring erectile function in diabetes. |
| 914 | 15184671 | RhoA/Rho-kinase suppresses endothelial nitric oxide synthase in the penis: a mechanism for diabetes-associated erectile dysfunction. |
| 915 | 15184671 | RhoA/Rho-kinase may suppress endothelial nitric oxide synthase (eNOS). |
| 916 | 15184671 | Here, we tested the hypothesis that RhoA/Rho-kinase contributes to diabetes-related erectile dysfunction and down-regulation of eNOS in the streptozotocin (STZ)-diabetic rat penis. |
| 917 | 15184671 | Colocalization of Rho-kinase and eNOS protein was present in the endothelium of the corpus cavernosum. |
| 918 | 15184671 | RhoA/Rho-kinase protein abundance and MYPT-1 phosphorylation at Thr-696 were elevated in the STZ-diabetic rat penis. |
| 919 | 15184671 | In addition, eNOS protein expression, cavernosal constitutive NOS activity, and cGMP levels were reduced in the STZ-diabetic penis. |
| 920 | 15184671 | To assess the functional role of RhoA/Rho-kinase in the penis, we evaluated the effects of an adeno-associated virus encoding the dominant-negative RhoA mutant (AAVTCMV19NRhoA) on RhoA/Rho-kinase and eNOS and erectile function in vivo in the STZ-diabetic rat. |
| 921 | 15184671 | STZ-diabetic rats transfected with AAVCMVT19NRhoA had a reduction in RhoA/Rho-kinase and MYPT-1 phosphorylation at a time when cavernosal eNOS protein, constitutive NOS activity, and cGMP levels were restored to levels found in the control rats. |
| 922 | 15184671 | These data demonstrate a previously undescribed mechanism for the down-regulation of penile eNOS in diabetes mediated by activation of the RhoA/Rho-kinase pathway. |
| 923 | 15184671 | Importantly, these data imply that inhibition of RhoA/Rho-kinase improves eNOS protein content and activity thus restoring erectile function in diabetes. |
| 924 | 15213066 | Dysregulation of kidney nitric oxide synthase (NOS) I may alter renal hemodynamics in diabetes. |
| 925 | 15224136 | Decreased expression or activity of neuronal or endothelial NO synthase (NOS), impaired NO release, or NO destruction will preclude sufficient cGMP formation to permit PDE5 inhibitor efficacy. |
| 926 | 15252773 | Based on the current evidence, it is reasonable to conclude that early nephropathy in diabetes is associated with increased intrarenal NO production mediated primarily by constitutively released NO (endothelial nitric oxide synthase [eNOS] and neuronal nitric oxide synthase [nNOS]). |
| 927 | 15252773 | Several factors including hyperglycemia, advanced glycosylation end products, increased oxidant stress, as well as activation of protein kinase C and transforming growth factor (TGF)-beta contribute to decreased NO production and/or availability. |
| 928 | 15261967 | We examined the electrostimulated penile responses, expression and activity of three enzymes: neuronal NO synthase (nNOS), endothelial NO synthase (eNOS) and caveolin-1 (CaV-1), and cGMP concentration that act upon the major NO-cGMP signaling pathways in penile tissue. |
| 929 | 15261967 | Furthermore, the penile expression levels of nNOS, eNOS and CaV-1, Ca2+ -dependent NOS activities and cGMP concentrations were increased significantly in the HF-treated rats. |
| 930 | 15261967 | We examined the electrostimulated penile responses, expression and activity of three enzymes: neuronal NO synthase (nNOS), endothelial NO synthase (eNOS) and caveolin-1 (CaV-1), and cGMP concentration that act upon the major NO-cGMP signaling pathways in penile tissue. |
| 931 | 15261967 | Furthermore, the penile expression levels of nNOS, eNOS and CaV-1, Ca2+ -dependent NOS activities and cGMP concentrations were increased significantly in the HF-treated rats. |
| 932 | 15292102 | Endothelial nitric oxide synthase (eNOS) and angiotensin-converting enzyme (ACE) polymorphisms have been associated with endothelial dysfunction, which is described as a cause of erectile dysfunction (ED). |
| 933 | 15292102 | Endothelial NOS and ACE are both regulators of vascular and corporal smooth muscle tone, which are connected by interaction between the NO-cyclic guanosine monophosphate pathway and the renin-angiotensin system. |
| 934 | 15292102 | We analyzed the frequencies of 894 G/T (Glu298Asp) eNOS and ACE I/D polymorphisms in Mexican patients with ED (n=53) and in an age-matched control group (n=62). |
| 935 | 15292117 | Penile tissue was evaluated for neuronal NO synthase (nNOS), smooth muscle alpha-actin, nitrotyrosine, and endothelial cell integrity. |
| 936 | 15328066 | To explore the participation of nitric oxide (NO) and caveolin-1 in this protective effect, we evaluated proteinuria, creatinine clearance, renal structural lesions, nitrites and nitrates urinary excretion (UNO(2)(-)/NO(3)V), and mRNA and protein levels of neuronal NO synthase (nNOS), endothelial NOS (eNOS), and caveolin-1 in lean and fatty Zucker rats fed with 20% casein or soy protein diet. |
| 937 | 15328066 | After 160 days of feeding with casein, fatty Zucker rats developed renal insufficiency, progressive proteinuria, and renal structural lesions; these alterations were associated with an important fall of UNO(2)(-)/NO(3)V, changes in nNOS and eNOS mRNA levels, together with increased amount of eNOS and caveolin-1 present in plasma membrane proteins of the kidney. |
| 938 | 15328066 | Renal protection was associated with reduction of caveolin-1 and eNOS in renal plasma membrane proteins. |
| 939 | 15328066 | To explore the participation of nitric oxide (NO) and caveolin-1 in this protective effect, we evaluated proteinuria, creatinine clearance, renal structural lesions, nitrites and nitrates urinary excretion (UNO(2)(-)/NO(3)V), and mRNA and protein levels of neuronal NO synthase (nNOS), endothelial NOS (eNOS), and caveolin-1 in lean and fatty Zucker rats fed with 20% casein or soy protein diet. |
| 940 | 15328066 | After 160 days of feeding with casein, fatty Zucker rats developed renal insufficiency, progressive proteinuria, and renal structural lesions; these alterations were associated with an important fall of UNO(2)(-)/NO(3)V, changes in nNOS and eNOS mRNA levels, together with increased amount of eNOS and caveolin-1 present in plasma membrane proteins of the kidney. |
| 941 | 15328066 | Renal protection was associated with reduction of caveolin-1 and eNOS in renal plasma membrane proteins. |
| 942 | 15383397 | Renal medullary NOS1 and NOS2 activities did not differ between groups, whereas NOS3 activity was significantly increased in Hyp. |
| 943 | 15383397 | Neither NOS1 nor NOS3 protein levels differed significantly between groups. |
| 944 | 15383397 | Immunohistochemical analysis indicated prominent expression of pThr(495)NOS3 in the thick ascending limb and collecting duct of Sham and Phz rats. |
| 945 | 15383397 | Renal medullary NOS1 and NOS2 activities did not differ between groups, whereas NOS3 activity was significantly increased in Hyp. |
| 946 | 15383397 | Neither NOS1 nor NOS3 protein levels differed significantly between groups. |
| 947 | 15383397 | Immunohistochemical analysis indicated prominent expression of pThr(495)NOS3 in the thick ascending limb and collecting duct of Sham and Phz rats. |
| 948 | 15481640 | Nitric oxide (NO) is synthesized from L-arginine by nitric oxide synthase (NOS). |
| 949 | 15481640 | In this study, the effect of Ginseng radix on the NOS expression in the hippocampus of streptozotocin (STZ)-induced diabetic rats was investigated via nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry. |
| 950 | 15481640 | Nitric oxide (NO) is synthesized from L-arginine by nitric oxide synthase (NOS). |
| 951 | 15481640 | In this study, the effect of Ginseng radix on the NOS expression in the hippocampus of streptozotocin (STZ)-induced diabetic rats was investigated via nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry. |
| 952 | 15501531 | In basilar arteries isolated from diabetic rats: (a) the ET-1-induced contraction was enhanced, (b) the contraction induced by N(G)-nitro-l-arginine [a nitric oxide synthase (NOS) inhibitor] was weaker, and (c) the levels of the mRNAs for ET(A)/ET(B) receptors and prepro-ET-1, but not for NOS, were significantly elevated (all versus age-matched controls). |
| 953 | 15524164 | Administration of tetrahydrobiopterin, an important co-factor for the enzyme nitric oxide synthase (NOS), has been demonstrated to enhance NO production in prehypertensive rats, restore endothelium-dependent vasodilatation in coronary arteries following reperfusion injury, aortae from streptozotocin-induced diabetic rats and in patients with hypercholesterolemia. |
| 954 | 15562034 | Insulin resistance is associated with impaired nitric oxide synthase activity in skeletal muscle of type 2 diabetic subjects. |
| 955 | 15562034 | We determined nitric oxide synthase (NOS) activity in skeletal muscle of 10 type 2 diabetic (hemoglobin A(1C) = 6.8 +/- 0.1%) and 11 control subjects under basal conditions and during an 80 mU/m(2).min euglycemic insulin clamp performed with vastus lateralis muscle biopsies before and after 4 h of insulin. |
| 956 | 15562034 | In response to insulin, NOS activity increased 2.5-fold in controls after 4 h (934 +/- 282 pmol/min.mg protein, P < 0.05 vs. basal), whereas insulin failed to stimulate NOS activity in diabetics (86 +/- 28 pmol/min.mg protein, P = NS from basal). |
| 957 | 15562034 | In controls, insulin-stimulated NOS activity correlated inversely with fasting plasma insulin concentration (r = -0.58, P = 0.05) and positively with Rd (r = 0.71, P = 0.03). |
| 958 | 15562034 | In control and diabetic groups collectively, Rd correlated with insulin-stimulated NOS activity (r = 0.52, P = 0.02). |
| 959 | 15562034 | We conclude that basal and insulin-stimulated muscle NOS activity is impaired in well-controlled type 2 diabetic subjects, and the defect in insulin-stimulated NOS activity correlates closely with the severity of insulin resistance. |
| 960 | 15562034 | These results suggest that impaired NOS activity may play an important role in the insulin resistance in type 2 diabetic individuals. |
| 961 | 15562034 | Insulin resistance is associated with impaired nitric oxide synthase activity in skeletal muscle of type 2 diabetic subjects. |
| 962 | 15562034 | We determined nitric oxide synthase (NOS) activity in skeletal muscle of 10 type 2 diabetic (hemoglobin A(1C) = 6.8 +/- 0.1%) and 11 control subjects under basal conditions and during an 80 mU/m(2).min euglycemic insulin clamp performed with vastus lateralis muscle biopsies before and after 4 h of insulin. |
| 963 | 15562034 | In response to insulin, NOS activity increased 2.5-fold in controls after 4 h (934 +/- 282 pmol/min.mg protein, P < 0.05 vs. basal), whereas insulin failed to stimulate NOS activity in diabetics (86 +/- 28 pmol/min.mg protein, P = NS from basal). |
| 964 | 15562034 | In controls, insulin-stimulated NOS activity correlated inversely with fasting plasma insulin concentration (r = -0.58, P = 0.05) and positively with Rd (r = 0.71, P = 0.03). |
| 965 | 15562034 | In control and diabetic groups collectively, Rd correlated with insulin-stimulated NOS activity (r = 0.52, P = 0.02). |
| 966 | 15562034 | We conclude that basal and insulin-stimulated muscle NOS activity is impaired in well-controlled type 2 diabetic subjects, and the defect in insulin-stimulated NOS activity correlates closely with the severity of insulin resistance. |
| 967 | 15562034 | These results suggest that impaired NOS activity may play an important role in the insulin resistance in type 2 diabetic individuals. |
| 968 | 15562034 | Insulin resistance is associated with impaired nitric oxide synthase activity in skeletal muscle of type 2 diabetic subjects. |
| 969 | 15562034 | We determined nitric oxide synthase (NOS) activity in skeletal muscle of 10 type 2 diabetic (hemoglobin A(1C) = 6.8 +/- 0.1%) and 11 control subjects under basal conditions and during an 80 mU/m(2).min euglycemic insulin clamp performed with vastus lateralis muscle biopsies before and after 4 h of insulin. |
| 970 | 15562034 | In response to insulin, NOS activity increased 2.5-fold in controls after 4 h (934 +/- 282 pmol/min.mg protein, P < 0.05 vs. basal), whereas insulin failed to stimulate NOS activity in diabetics (86 +/- 28 pmol/min.mg protein, P = NS from basal). |
| 971 | 15562034 | In controls, insulin-stimulated NOS activity correlated inversely with fasting plasma insulin concentration (r = -0.58, P = 0.05) and positively with Rd (r = 0.71, P = 0.03). |
| 972 | 15562034 | In control and diabetic groups collectively, Rd correlated with insulin-stimulated NOS activity (r = 0.52, P = 0.02). |
| 973 | 15562034 | We conclude that basal and insulin-stimulated muscle NOS activity is impaired in well-controlled type 2 diabetic subjects, and the defect in insulin-stimulated NOS activity correlates closely with the severity of insulin resistance. |
| 974 | 15562034 | These results suggest that impaired NOS activity may play an important role in the insulin resistance in type 2 diabetic individuals. |
| 975 | 15562034 | Insulin resistance is associated with impaired nitric oxide synthase activity in skeletal muscle of type 2 diabetic subjects. |
| 976 | 15562034 | We determined nitric oxide synthase (NOS) activity in skeletal muscle of 10 type 2 diabetic (hemoglobin A(1C) = 6.8 +/- 0.1%) and 11 control subjects under basal conditions and during an 80 mU/m(2).min euglycemic insulin clamp performed with vastus lateralis muscle biopsies before and after 4 h of insulin. |
| 977 | 15562034 | In response to insulin, NOS activity increased 2.5-fold in controls after 4 h (934 +/- 282 pmol/min.mg protein, P < 0.05 vs. basal), whereas insulin failed to stimulate NOS activity in diabetics (86 +/- 28 pmol/min.mg protein, P = NS from basal). |
| 978 | 15562034 | In controls, insulin-stimulated NOS activity correlated inversely with fasting plasma insulin concentration (r = -0.58, P = 0.05) and positively with Rd (r = 0.71, P = 0.03). |
| 979 | 15562034 | In control and diabetic groups collectively, Rd correlated with insulin-stimulated NOS activity (r = 0.52, P = 0.02). |
| 980 | 15562034 | We conclude that basal and insulin-stimulated muscle NOS activity is impaired in well-controlled type 2 diabetic subjects, and the defect in insulin-stimulated NOS activity correlates closely with the severity of insulin resistance. |
| 981 | 15562034 | These results suggest that impaired NOS activity may play an important role in the insulin resistance in type 2 diabetic individuals. |
| 982 | 15562034 | Insulin resistance is associated with impaired nitric oxide synthase activity in skeletal muscle of type 2 diabetic subjects. |
| 983 | 15562034 | We determined nitric oxide synthase (NOS) activity in skeletal muscle of 10 type 2 diabetic (hemoglobin A(1C) = 6.8 +/- 0.1%) and 11 control subjects under basal conditions and during an 80 mU/m(2).min euglycemic insulin clamp performed with vastus lateralis muscle biopsies before and after 4 h of insulin. |
| 984 | 15562034 | In response to insulin, NOS activity increased 2.5-fold in controls after 4 h (934 +/- 282 pmol/min.mg protein, P < 0.05 vs. basal), whereas insulin failed to stimulate NOS activity in diabetics (86 +/- 28 pmol/min.mg protein, P = NS from basal). |
| 985 | 15562034 | In controls, insulin-stimulated NOS activity correlated inversely with fasting plasma insulin concentration (r = -0.58, P = 0.05) and positively with Rd (r = 0.71, P = 0.03). |
| 986 | 15562034 | In control and diabetic groups collectively, Rd correlated with insulin-stimulated NOS activity (r = 0.52, P = 0.02). |
| 987 | 15562034 | We conclude that basal and insulin-stimulated muscle NOS activity is impaired in well-controlled type 2 diabetic subjects, and the defect in insulin-stimulated NOS activity correlates closely with the severity of insulin resistance. |
| 988 | 15562034 | These results suggest that impaired NOS activity may play an important role in the insulin resistance in type 2 diabetic individuals. |
| 989 | 15562034 | Insulin resistance is associated with impaired nitric oxide synthase activity in skeletal muscle of type 2 diabetic subjects. |
| 990 | 15562034 | We determined nitric oxide synthase (NOS) activity in skeletal muscle of 10 type 2 diabetic (hemoglobin A(1C) = 6.8 +/- 0.1%) and 11 control subjects under basal conditions and during an 80 mU/m(2).min euglycemic insulin clamp performed with vastus lateralis muscle biopsies before and after 4 h of insulin. |
| 991 | 15562034 | In response to insulin, NOS activity increased 2.5-fold in controls after 4 h (934 +/- 282 pmol/min.mg protein, P < 0.05 vs. basal), whereas insulin failed to stimulate NOS activity in diabetics (86 +/- 28 pmol/min.mg protein, P = NS from basal). |
| 992 | 15562034 | In controls, insulin-stimulated NOS activity correlated inversely with fasting plasma insulin concentration (r = -0.58, P = 0.05) and positively with Rd (r = 0.71, P = 0.03). |
| 993 | 15562034 | In control and diabetic groups collectively, Rd correlated with insulin-stimulated NOS activity (r = 0.52, P = 0.02). |
| 994 | 15562034 | We conclude that basal and insulin-stimulated muscle NOS activity is impaired in well-controlled type 2 diabetic subjects, and the defect in insulin-stimulated NOS activity correlates closely with the severity of insulin resistance. |
| 995 | 15562034 | These results suggest that impaired NOS activity may play an important role in the insulin resistance in type 2 diabetic individuals. |
| 996 | 15576299 | Asymmetric dimethylarginine (ADMA) is an endogenous competitive inhibitor of nitric oxide synthase (NOS). |
| 997 | 15582161 | Expression of the axotomy-responsive genes coding for growth-associated protein 43 (GAP-43), galanin, neuropeptide Y (NPY), pre-pro-vasoactive intestinal polypeptide (pre-pro-VIP), neuronal nitric oxide synthase (nNOS), protease nexin 1, heat-shock protein 27 (HSP 27) and myosin light chain kinase II (MLCK II) was unaffected in ganglia from diabetic rats compared to controls; thus, no axotomised phenotype was established. |
| 998 | 15582161 | The expression of the majority of proapoptotic genes in the DRG was also unaltered (bax, bad, bid, bok, c-Jun, p38, TNFR1, caspase 3 and NOS2). |
| 999 | 15582161 | Similarly there was no change in expression of the majority of antiapoptotic genes (bcl2, bcl-xL, bcl-w, NfkappaB). |
| 1000 | 15582286 | Based on animal and cell studies, neurogenic ED is assumed to be caused mainly by: (a) an insufficient synthesis of nitric oxide (NO) due to a decrease in the levels of the penile neuronal nitric oxide synthase (PnNOS) or the impairment of its regulation by protein effectors (NMDA receptor, protein inhibitor of nNOS: PIN), occurring in the neuronal bodies or nerve terminals, or (b) a loss of the cells themselves by apoptosis caused by the induction of inducible NOS (iNOS) and the production of peroxynitrite. |
| 1001 | 15582286 | In contrast vasculogenic ED, although may involve endothelial damage and down-regulation of endothelial NOS (eNOS), appears to be mainly caused by the relative loss of smooth muscle cells and replacement by collagen fibers (fibrosis) that impairs tissue compliance. |
| 1002 | 15582286 | In this case, iNOS induction may not be deleterious, but a defense mechanism preventing excessive collagen deposition. |
| 1003 | 15582286 | Based on animal and cell studies, neurogenic ED is assumed to be caused mainly by: (a) an insufficient synthesis of nitric oxide (NO) due to a decrease in the levels of the penile neuronal nitric oxide synthase (PnNOS) or the impairment of its regulation by protein effectors (NMDA receptor, protein inhibitor of nNOS: PIN), occurring in the neuronal bodies or nerve terminals, or (b) a loss of the cells themselves by apoptosis caused by the induction of inducible NOS (iNOS) and the production of peroxynitrite. |
| 1004 | 15582286 | In contrast vasculogenic ED, although may involve endothelial damage and down-regulation of endothelial NOS (eNOS), appears to be mainly caused by the relative loss of smooth muscle cells and replacement by collagen fibers (fibrosis) that impairs tissue compliance. |
| 1005 | 15582286 | In this case, iNOS induction may not be deleterious, but a defense mechanism preventing excessive collagen deposition. |
| 1006 | 15629260 | The results show that EEP and WSD led to decreased levels of blood glucose (FBG), fructosamine (FRU), malonaldehyde (MDA), nitric oxide (NO), nitric oxide synthetase (NOS), total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), very low-density lipoprotein cholesterol (VLDL-C) in serum of fasting rats; and to increased serum levels of high-density lipoprotein cholesterol (HDL-C) and superoxide dismutase (SOD). |
| 1007 | 15635855 | Apart from its effect on the cardiovascular system it exerts an effect also on other types of cells and ensures their functions.Specially comprehensive is its synthesis and action in the kidneys: NO is formed in the endothelial cells due to the activity of constitutional endothelial synthase (eNOS), in mesangial cells of inductive synthase (iNOS), in smooth muscle cells (vsmNOS), in tubular cells neuronal NOS (nNOS) and iNOS and in the macula densa nNOS. |
| 1008 | 15687247 | The mRNA and protein expression of endothelial NOS (eNOS), as measured by real-time RT-PCR and Western blotting, increased significantly (mRNA level, 1.3-fold; protein level, 1.8-fold). |
| 1009 | 15722114 | Nitric oxide (NO) is a gaseous lipophilic free radical cellular messenger generated by three distinct isoforms of nitric oxide synthases (NOS), neuronal (nNOS), inducible (iNOS) and endothelial NOS (eNOS). |
| 1010 | 15753231 | In this regard, substrate and cofactor availability play important roles in regulating nitric oxide synthase (NOS) activity not only by limiting enzyme activity but also by influencing the coupling of NOS with its cofactors, tetrahydrobiopterin and NADPH. |
| 1011 | 15774613 | Plasma levels of nitrite ions have been used as an index of nitric oxide synthase (NOS) activity in vivo. |
| 1012 | 15777779 | Immunoblotting and high-performance liquid chromatography (HPLC)-based techniques revealed, respectively, that the above inverse relationship between O2- and NO was associated with a marked increase in the protein expression of nitric oxide synthase (eNOS) and a decrease in the level of its cofactor tetrahydrobiopterin (BH4) in diabetic aortas. |
| 1013 | 15777779 | Our studies suggest that diabetes produces a cascade of events involving production of reactive oxygen species from the NADPH oxidase leading to oxidation of BH4 and uncoupling of NOS. |
| 1014 | 15795174 | Choline acetyltransferase and inducible nitric oxide synthase are increased in myenteric plexus of diabetic guinea pig. |
| 1015 | 15795174 | After 5-6 weeks, expressions of choline acetyltransferase, neuronal nitric oxide synthase and inducible nitric oxide synthase were determined in longitudinal and myenteric plexus preparations using indirect immunohistochemistry. |
| 1016 | 15795174 | In ileum from streptozotocin-treated animals, the density of choline acetyltransferase-immunoreactive nerve fibers within the tertiary plexus and the percent total myenteric neurons expressing inducible nitric oxide synthase were increased, but the percent total myenteric neurons expressing neuronal nitric oxide synthase was not changed. |
| 1017 | 15795174 | Choline acetyltransferase and inducible nitric oxide synthase are increased in myenteric plexus of diabetic guinea pig. |
| 1018 | 15795174 | After 5-6 weeks, expressions of choline acetyltransferase, neuronal nitric oxide synthase and inducible nitric oxide synthase were determined in longitudinal and myenteric plexus preparations using indirect immunohistochemistry. |
| 1019 | 15795174 | In ileum from streptozotocin-treated animals, the density of choline acetyltransferase-immunoreactive nerve fibers within the tertiary plexus and the percent total myenteric neurons expressing inducible nitric oxide synthase were increased, but the percent total myenteric neurons expressing neuronal nitric oxide synthase was not changed. |
| 1020 | 15830095 | Rosiglitazone (ROSI), thiazolidione peroxisome proliferator-activated receptor-gamma (PPAR-gamma) activator, reduces insulin resistance in patients with type 2 diabetes (T2DM). |
| 1021 | 15830095 | To explore the mechanism, nitric oxide synthase (NOS) inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) was used and serum nitric oxide (NO) was measured. |
| 1022 | 15830095 | These findings suggest that ROSI can improve aortic diastolic function of insulin resistant-hypertensive rats, the mechanism of this effect might be associated with an increase in nitric oxide mediated partly by NOS pathway, a decrease in the level of blood pressure, serum insulin and the improvement of insulin resistance. |
| 1023 | 15830095 | Rosiglitazone (ROSI), thiazolidione peroxisome proliferator-activated receptor-gamma (PPAR-gamma) activator, reduces insulin resistance in patients with type 2 diabetes (T2DM). |
| 1024 | 15830095 | To explore the mechanism, nitric oxide synthase (NOS) inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) was used and serum nitric oxide (NO) was measured. |
| 1025 | 15830095 | These findings suggest that ROSI can improve aortic diastolic function of insulin resistant-hypertensive rats, the mechanism of this effect might be associated with an increase in nitric oxide mediated partly by NOS pathway, a decrease in the level of blood pressure, serum insulin and the improvement of insulin resistance. |
| 1026 | 15856945 | The allele and genotype frequencies of polymorphic markers of NOS1, NOS2 and NOS3 genes, encoding three types of NO synthases, were compared in type 1 diabetes patients with and without diabetic polyneuropathty. 180 type 1 diabetes patients (T1DM) of Russian or Eastern Slavonic origin, living in Moscow city, were divided into two groups using non-overlapping (polar) phenotypes. 86 patients had overt DPN and T1DM duration in this group was less than 5 years (DPN+ group) and 94 patients had no clinical DPN and T1DM duration was more than 10 years (DPN- group). |
| 1027 | 15856945 | We have not found the significant differences of allele and genotype frequencies of polymorphic markers (CA)n of NOS1 gene, (CCTTT)n of NOS2 gene, ecNOS4a/4b and Glu298Asp of NOS3 gene that indicates that all these markers are not associated with diabetic polyneuropathty. |
| 1028 | 15856945 | The allele and genotype frequencies of polymorphic markers of NOS1, NOS2 and NOS3 genes, encoding three types of NO synthases, were compared in type 1 diabetes patients with and without diabetic polyneuropathty. 180 type 1 diabetes patients (T1DM) of Russian or Eastern Slavonic origin, living in Moscow city, were divided into two groups using non-overlapping (polar) phenotypes. 86 patients had overt DPN and T1DM duration in this group was less than 5 years (DPN+ group) and 94 patients had no clinical DPN and T1DM duration was more than 10 years (DPN- group). |
| 1029 | 15856945 | We have not found the significant differences of allele and genotype frequencies of polymorphic markers (CA)n of NOS1 gene, (CCTTT)n of NOS2 gene, ecNOS4a/4b and Glu298Asp of NOS3 gene that indicates that all these markers are not associated with diabetic polyneuropathty. |
| 1030 | 15890370 | Nitric oxide (NO) is a potent regulator in the cardiovascular system; it is generated by the nitric oxide synthase (NOS) family of proteins. |
| 1031 | 15890370 | Aortic NO metabolities (nitrite/nitrate) and endothelial NOS (NOS-3) were assayed by Griess reaction and by immunoblotting and immunohistochemistry, respectively. |
| 1032 | 15890370 | Nitric oxide (NO) is a potent regulator in the cardiovascular system; it is generated by the nitric oxide synthase (NOS) family of proteins. |
| 1033 | 15890370 | Aortic NO metabolities (nitrite/nitrate) and endothelial NOS (NOS-3) were assayed by Griess reaction and by immunoblotting and immunohistochemistry, respectively. |
| 1034 | 15933265 | Hypoxia also reduced hENT1 protein and mRNA levels, effects unaltered by N(omega)-nitro-l-arginine methyl ester (l-NAME, nitric oxide synthase [NOS] inhibitor) or PD-98059 (inhibitor of mitogen-activated protein kinase kinase 1 and 2 [MEK1/2]). |
| 1035 | 15933265 | Hypoxia reduced endothelial NOS (eNOS) activity and eNOS phosphorylation at Ser(1177), but increased eNOS protein level. |
| 1036 | 15933265 | Hypoxia also reduced hENT1 protein and mRNA levels, effects unaltered by N(omega)-nitro-l-arginine methyl ester (l-NAME, nitric oxide synthase [NOS] inhibitor) or PD-98059 (inhibitor of mitogen-activated protein kinase kinase 1 and 2 [MEK1/2]). |
| 1037 | 15933265 | Hypoxia reduced endothelial NOS (eNOS) activity and eNOS phosphorylation at Ser(1177), but increased eNOS protein level. |
| 1038 | 15964597 | We also determined the total nitric oxide synthase (NOS) activity (conversion of L-arginine to citrulline) and endothelial(e), inducible(i), and neuronal(n) NOS expression (using polymerase chain reaction after reverse transcription of the mRNAs into cDNAs) in the mesentery of metformin-treated n-STZ diabetic and vehicle-treated n-STZ diabetic and control rats. |
| 1039 | 15967436 | Non-diabetic and diabetic (treated with streptozotocin 65 mg kg(-1) body wt, i.p.) rats were injected with the nitric oxide synthase (NOS) inhibitor, L-NAME (50 mg kg(-1) body wt day(-1), x 10 days i.p.) or NOS substrate, L-arginine (200 mg kg(-1) body wt day(-1), x 10 days i.p.). |
| 1040 | 15981946 | PKC may have multiple adverse effects on vascular function, including the activation of superoxide-producing enzymes such as the nicotinamide adenine dinicleotide phosphate (NADPH) oxidase as well as increased expression of a dysfunctional, superoxide-producing, uncoupled endothelial nitric oxide synthase (NOS III). |
| 1041 | 15983249 | Neuronal nitric oxide synthase mediates statin-induced restoration of vasa nervorum and reversal of diabetic neuropathy. |
| 1042 | 16022682 | NOS activity was measured from the conversion of L-[(3)H]arginine into L-[(3)H]citrulline, and the expression, serine phosphorylation and O-glycosylation of NOS-3 were determined by Western blotting. |
| 1043 | 16022682 | By contrast, AGE-modified albumin exerted a concentration- and time-dependent suppression of NOS-3 expression in HUVECs at a range of concentrations (0-200 mg/l) found in diabetic plasma; this was evident after 24 h, whereas inhibition of NOS activity was seen after only 3 h incubation with AGE-modified albumin, consistent with our previous observations of rapid suppression of NOS-3 serine phosphorylation and NOS-3 activity by AGE-modified albumin. |
| 1044 | 16022682 | In conclusion, AGE-modified albumin suppresses NOS-3 activity in HUVECs through two mechanisms: one rapid, involving suppression of its serine phosphorylation, and another slower, involving a decrease in its expression. |
| 1045 | 16022682 | NOS activity was measured from the conversion of L-[(3)H]arginine into L-[(3)H]citrulline, and the expression, serine phosphorylation and O-glycosylation of NOS-3 were determined by Western blotting. |
| 1046 | 16022682 | By contrast, AGE-modified albumin exerted a concentration- and time-dependent suppression of NOS-3 expression in HUVECs at a range of concentrations (0-200 mg/l) found in diabetic plasma; this was evident after 24 h, whereas inhibition of NOS activity was seen after only 3 h incubation with AGE-modified albumin, consistent with our previous observations of rapid suppression of NOS-3 serine phosphorylation and NOS-3 activity by AGE-modified albumin. |
| 1047 | 16022682 | In conclusion, AGE-modified albumin suppresses NOS-3 activity in HUVECs through two mechanisms: one rapid, involving suppression of its serine phosphorylation, and another slower, involving a decrease in its expression. |
| 1048 | 16024729 | Nephrogenic diabetes insipidus in mice lacking all nitric oxide synthase isoforms. |
| 1049 | 16024729 | In the kidney of the triply NOS-/- mice, vasopressin-induced cAMP production and membranous aquaporin-2 water channel expression were reduced associated with tubuloglomerular lesion formation. |
| 1050 | 16045816 | Left ventricular tissue was processed for enzyme catalytic histochemistry of capillary alkaline phosphatase (AlPh), dipeptidyl peptidase IV (DPP IV), and endothelial NO synthase/NADPH-diaphorase (NOS) and for ultrastructural analysis. |
| 1051 | 16045816 | Quantitative evaluation demonstrated reduction of reaction product intensity of AlPh, DPP and NOS by 49.50%, 74.36%, 20.05% in diabetic and 62.93%, 82.71%, 37.65% in hypertensive rats. |
| 1052 | 16077883 | Three isoforms of this enzyme were discovered and cloned: a constitutive neuronal isoform (nNOS); an inducible isoform (iNOS), ubiquitous in cells stimulated by certain cytokines; and an endothelial isoform (eNOS). |
| 1053 | 16120812 | Absence of a dilatory effect in endothelial nitric-oxide synthase (NOS) -/- mice suggests endothelial NOS as the source of NO. |
| 1054 | 16160603 | Nitric oxide synthase (NOS) uncoupling is a condition of increased production of superoxide anion associated with a decreased production of nitric oxide (NO) by this enzyme. |
| 1055 | 16230278 | Several mechanisms have been proposed to explain this "arginine paradox": co-localization of the arginine transporter with endothelial nitric oxide synthase, intracellular arginine regeneration from citrulline, balance between endothelial arginase and nitric oxide synthase. |
| 1056 | 16230278 | The co-operation between cholesterol synthesis and the upregulation of caveolin-1 on the one hand, and the activation of endothelial nitric oxide synthase on the other hand, is very tight. |
| 1057 | 16230278 | A depletion of cholesterol in the caveolae induces a decrease in caveolin-1 at the cell surface allowing NOS activation. |
| 1058 | 16231005 | Endothelial NOS was increased but SK2, SK3 and connexin (Cx) 37 mRNA expressions were significantly (P<0.05) decreased in the SMA from STZ-treated apoE-deficient mice compared to the CIT-treated controls. |
| 1059 | 16231005 | The microvasculature of STZ-induced apoE-deficient mice developed endothelial dysfunction, which may be linked to a decrease in the contribution of the EDHF component due to a decrease in SK2 and 3 and Cx 37 expression. |
| 1060 | 16232352 | Pravastatin activates platelet nitric oxide synthase (NOS) in patients with type 2 diabetes mellitus and NOS activation is accompanied by serine phosphorylation. |
| 1061 | 16234413 | In endothelial cells, S1P has been shown to modulate the activity of the endothelial nitric-oxide synthase (eNOS) through phosphorylation operated by Akt. |
| 1062 | 16234413 | Nitric oxide (NO) produced by neuronal nitric-oxide synthase and eNOS plays a central role in triggering and maintaining penile erection. |
| 1063 | 16234413 | This study has assessed the possibility of a similar cross-talk between eNOS and S1P in human corpus cavernosum and whether this interaction is connected to penile vascular response. |
| 1064 | 16234413 | Quantitative reverse transcription-polymerase chain reaction demonstrated the presence of S1P(1), S1P(2), and S1P(3) receptors in both the human corpus cavernosum (HCC) and the penile artery. |
| 1065 | 16234413 | In human tissue, S1P seems to be the possible candidate for the activation of the eNOS calcium-independent pathway. |
| 1066 | 16256381 | Here, we investigated the role of nitric oxide (NO) and nitric oxide synthase (NOS) isoforms on glibenclamide-induced apoptosis in rat insulinoma cells. |
| 1067 | 16256381 | The effects of glibenclamide on cell viability were partially inhibited after treatment with N(G)-nitro-L-arginine methyl ester (L-NAME), inhibitor more selective for constitutive nitric oxide synthase, and in the presence of D600--a blocker of voltage-gated L-type Ca(2+) channels inhibited Ca(2+) influx into beta cells, whereas aminoguanidine (AG), a preferential inhibitor of inducible NOS, was significantly less effective. |
| 1068 | 16256381 | Here, we investigated the role of nitric oxide (NO) and nitric oxide synthase (NOS) isoforms on glibenclamide-induced apoptosis in rat insulinoma cells. |
| 1069 | 16256381 | The effects of glibenclamide on cell viability were partially inhibited after treatment with N(G)-nitro-L-arginine methyl ester (L-NAME), inhibitor more selective for constitutive nitric oxide synthase, and in the presence of D600--a blocker of voltage-gated L-type Ca(2+) channels inhibited Ca(2+) influx into beta cells, whereas aminoguanidine (AG), a preferential inhibitor of inducible NOS, was significantly less effective. |
| 1070 | 16260352 | High serum TNF-alpha level in Type 2 diabetic patients with microangiopathy is associated with eNOS down-regulation and apoptosis in endothelial cells. |
| 1071 | 16260352 | Serum levels of TNF-alpha and vascular endothelial growth factor (VEGF) were elevated in diabetic patients. |
| 1072 | 16260352 | Plasma levels of TNF-alpha, two soluble TNF-alpha receptors (sTNFR), and VEGF were assessed in diabetic patients (CD, n=21) complicated with retinopathy and/or nephropathy, uncomplicated diabetic patients (UD, n=18), and in healthy normal participants (NS, n=16). |
| 1073 | 16260352 | In HUVECs incubated with patient's serum, endothelial constitutive nitric oxide synthase (eNOS) protein expressions were measured by Western blot analysis. |
| 1074 | 16260352 | Serum TNF-alpha, sTNFR-I, and asymmetric dimethylarginine (ADMA), an endogenous inhibitor of NOS, in CD were significantly higher than in UD or NS. |
| 1075 | 16260352 | While, serum sTNFR-I and VEGF levels were significantly increased in the both diabetic patients, compared with those of NS, no difference was observed in the serum TNF-alpha, sTNFR-II, and ADMA levels between UD and NS. eNOS down-regulation and apoptosis were seen in HUVECs incubated with serum from CD for 24 h, but those observations were completely counteracted in the incubation by the addition of the antihuman TNF-alpha antibody. |
| 1076 | 16260352 | These results imply that eNOS down-regulation in CD is associated with high serum TNF-alpha levels despite of high serum of VEGF levels. |
| 1077 | 16288928 | The aim of our experimental work was to test the effect of hyperglycemic state on the level of urinary stable NO end products and on the expression of inducible nitric oxide synthase (NOS II) in white blood cells (WBC). |
| 1078 | 16288928 | However, the increase of the activity and the expression of inducible NOS II were only observed in rat white blood cells and this effect was prevented by insulin treatment. |
| 1079 | 16288928 | In human samples, less than 25% of children showed elevated NOS II expression in white blood cells without any correlation to the level of urinary NO end products and glycated hemoglobin in blood. |
| 1080 | 16288928 | The aim of our experimental work was to test the effect of hyperglycemic state on the level of urinary stable NO end products and on the expression of inducible nitric oxide synthase (NOS II) in white blood cells (WBC). |
| 1081 | 16288928 | However, the increase of the activity and the expression of inducible NOS II were only observed in rat white blood cells and this effect was prevented by insulin treatment. |
| 1082 | 16288928 | In human samples, less than 25% of children showed elevated NOS II expression in white blood cells without any correlation to the level of urinary NO end products and glycated hemoglobin in blood. |
| 1083 | 16288928 | The aim of our experimental work was to test the effect of hyperglycemic state on the level of urinary stable NO end products and on the expression of inducible nitric oxide synthase (NOS II) in white blood cells (WBC). |
| 1084 | 16288928 | However, the increase of the activity and the expression of inducible NOS II were only observed in rat white blood cells and this effect was prevented by insulin treatment. |
| 1085 | 16288928 | In human samples, less than 25% of children showed elevated NOS II expression in white blood cells without any correlation to the level of urinary NO end products and glycated hemoglobin in blood. |
| 1086 | 16322352 | The change in number of NADPH-diaphorase-positive neurons [a marker for neuronal NO synthase (nNOS) activity] in the PVN was measured. |
| 1087 | 16323284 | Expression of the skeletal muscle dystrophin-dystroglycan complex and syntrophin-nitric oxide synthase complex is severely affected in the type 2 diabetic Goto-Kakizaki rat. |
| 1088 | 16323284 | In addition, this analysis revealed an unexpected drastic reduction in the surface membrane marker beta-dystroglycan, a dystrophin-associated glycoprotein. |
| 1089 | 16323284 | Based on this finding, a comprehensive immunoblotting survey was conducted which showed a dramatic decrease in the Dp427 isoform of dystrophin and the alpha/beta-dystroglycan subcomplex, but not in laminin, sarcoglycans, dystrobrevin, and excitation-contraction-relaxation cycle elements. |
| 1090 | 16323284 | Most importantly, the expression of alpha-syntrophin and the syntrophin-associated neuronal isoform of nitric oxide synthase, nNOS, was demonstrated to be severely reduced in diabetic fibres. |
| 1091 | 16323284 | Impaired anchoring of the cortical actin cytoskeleton via dystrophin might interfere with the proper recruitment of the glucose transporter to the surface membrane, following stimulation by insulin or muscle contraction. |
| 1092 | 16372481 | Comparison of the control and diabetic groups revealed that the axons of nerve cells were not identified with Masson trichrome in the diabetic group, whereas in the control group NOS localization and immunostaining (endothelial NOS [eNOS]) were normal. |
| 1093 | 16372481 | Diabetic rats administered ALA showed improvement in Masson trichrome, nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) and eNOS localization compared with untreated diabetic rats. |
| 1094 | 16372481 | In erection, eNOS and neuronal NOS (nNOS) may have a significant role. |
| 1095 | 16372481 | In pathologic conditions, erectile dysfunction may occur as a result of an increase in inducible macrophage-type NOS (iNOS). |
| 1096 | 16372481 | ALA plays an important role in treatment of erectile dysfunction by decreasing iNOS and increasing other isoforms of NOS. |
| 1097 | 16372481 | Comparison of the control and diabetic groups revealed that the axons of nerve cells were not identified with Masson trichrome in the diabetic group, whereas in the control group NOS localization and immunostaining (endothelial NOS [eNOS]) were normal. |
| 1098 | 16372481 | Diabetic rats administered ALA showed improvement in Masson trichrome, nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) and eNOS localization compared with untreated diabetic rats. |
| 1099 | 16372481 | In erection, eNOS and neuronal NOS (nNOS) may have a significant role. |
| 1100 | 16372481 | In pathologic conditions, erectile dysfunction may occur as a result of an increase in inducible macrophage-type NOS (iNOS). |
| 1101 | 16372481 | ALA plays an important role in treatment of erectile dysfunction by decreasing iNOS and increasing other isoforms of NOS. |
| 1102 | 16372481 | Comparison of the control and diabetic groups revealed that the axons of nerve cells were not identified with Masson trichrome in the diabetic group, whereas in the control group NOS localization and immunostaining (endothelial NOS [eNOS]) were normal. |
| 1103 | 16372481 | Diabetic rats administered ALA showed improvement in Masson trichrome, nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) and eNOS localization compared with untreated diabetic rats. |
| 1104 | 16372481 | In erection, eNOS and neuronal NOS (nNOS) may have a significant role. |
| 1105 | 16372481 | In pathologic conditions, erectile dysfunction may occur as a result of an increase in inducible macrophage-type NOS (iNOS). |
| 1106 | 16372481 | ALA plays an important role in treatment of erectile dysfunction by decreasing iNOS and increasing other isoforms of NOS. |
| 1107 | 16372481 | Comparison of the control and diabetic groups revealed that the axons of nerve cells were not identified with Masson trichrome in the diabetic group, whereas in the control group NOS localization and immunostaining (endothelial NOS [eNOS]) were normal. |
| 1108 | 16372481 | Diabetic rats administered ALA showed improvement in Masson trichrome, nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) and eNOS localization compared with untreated diabetic rats. |
| 1109 | 16372481 | In erection, eNOS and neuronal NOS (nNOS) may have a significant role. |
| 1110 | 16372481 | In pathologic conditions, erectile dysfunction may occur as a result of an increase in inducible macrophage-type NOS (iNOS). |
| 1111 | 16372481 | ALA plays an important role in treatment of erectile dysfunction by decreasing iNOS and increasing other isoforms of NOS. |
| 1112 | 16375869 | Diabetes only affects nitric oxide synthase-containing myenteric neurons that do not contain heme oxygenase 2. |
| 1113 | 16375869 | Some of the nNOS-containing neurons also contain heme oxygenase 2 (HO2). |
| 1114 | 16375869 | Therefore, the aim of this study was to compare the effects of diabetes on HO2- and nNOS-containing neurons within the myenteric plexus of the rat ileum. |
| 1115 | 16375869 | After 12 weeks, immunostaining of wholemount preparations of ileum revealed that diabetes induced a significant shift (P < 0.001, chi-squared test for trend) towards increased neuronal cell body size in nNOS-immunoreactive neurons while HO2-immunoreactive neurons remained unaffected. |
| 1116 | 16375869 | Double-labeling studies revealed that approximately 50% of nNOS-containing neurons also contained HO2 and that the diabetes-induced change in size was confined to nNOS-immunoreactive neurons that did not contain HO2 (P < 0.01). |
| 1117 | 16375869 | No change in the size distribution occurred in neurons in which nNOS and HO2 were colocalized. |
| 1118 | 16375869 | Differences in the response of these two subpopulations of nNOS-containing neurons to diabetes could occur because they supply different targets within the gastrointestinal tract or indicate that the antioxidant, HO2, protects those nNOS-containing neurons in which it is colocalized, against oxidative stress that occurs in diabetes. |
| 1119 | 16375869 | Diabetes only affects nitric oxide synthase-containing myenteric neurons that do not contain heme oxygenase 2. |
| 1120 | 16375869 | Some of the nNOS-containing neurons also contain heme oxygenase 2 (HO2). |
| 1121 | 16375869 | Therefore, the aim of this study was to compare the effects of diabetes on HO2- and nNOS-containing neurons within the myenteric plexus of the rat ileum. |
| 1122 | 16375869 | After 12 weeks, immunostaining of wholemount preparations of ileum revealed that diabetes induced a significant shift (P < 0.001, chi-squared test for trend) towards increased neuronal cell body size in nNOS-immunoreactive neurons while HO2-immunoreactive neurons remained unaffected. |
| 1123 | 16375869 | Double-labeling studies revealed that approximately 50% of nNOS-containing neurons also contained HO2 and that the diabetes-induced change in size was confined to nNOS-immunoreactive neurons that did not contain HO2 (P < 0.01). |
| 1124 | 16375869 | No change in the size distribution occurred in neurons in which nNOS and HO2 were colocalized. |
| 1125 | 16375869 | Differences in the response of these two subpopulations of nNOS-containing neurons to diabetes could occur because they supply different targets within the gastrointestinal tract or indicate that the antioxidant, HO2, protects those nNOS-containing neurons in which it is colocalized, against oxidative stress that occurs in diabetes. |
| 1126 | 16375869 | Diabetes only affects nitric oxide synthase-containing myenteric neurons that do not contain heme oxygenase 2. |
| 1127 | 16375869 | Some of the nNOS-containing neurons also contain heme oxygenase 2 (HO2). |
| 1128 | 16375869 | Therefore, the aim of this study was to compare the effects of diabetes on HO2- and nNOS-containing neurons within the myenteric plexus of the rat ileum. |
| 1129 | 16375869 | After 12 weeks, immunostaining of wholemount preparations of ileum revealed that diabetes induced a significant shift (P < 0.001, chi-squared test for trend) towards increased neuronal cell body size in nNOS-immunoreactive neurons while HO2-immunoreactive neurons remained unaffected. |
| 1130 | 16375869 | Double-labeling studies revealed that approximately 50% of nNOS-containing neurons also contained HO2 and that the diabetes-induced change in size was confined to nNOS-immunoreactive neurons that did not contain HO2 (P < 0.01). |
| 1131 | 16375869 | No change in the size distribution occurred in neurons in which nNOS and HO2 were colocalized. |
| 1132 | 16375869 | Differences in the response of these two subpopulations of nNOS-containing neurons to diabetes could occur because they supply different targets within the gastrointestinal tract or indicate that the antioxidant, HO2, protects those nNOS-containing neurons in which it is colocalized, against oxidative stress that occurs in diabetes. |
| 1133 | 16375869 | Diabetes only affects nitric oxide synthase-containing myenteric neurons that do not contain heme oxygenase 2. |
| 1134 | 16375869 | Some of the nNOS-containing neurons also contain heme oxygenase 2 (HO2). |
| 1135 | 16375869 | Therefore, the aim of this study was to compare the effects of diabetes on HO2- and nNOS-containing neurons within the myenteric plexus of the rat ileum. |
| 1136 | 16375869 | After 12 weeks, immunostaining of wholemount preparations of ileum revealed that diabetes induced a significant shift (P < 0.001, chi-squared test for trend) towards increased neuronal cell body size in nNOS-immunoreactive neurons while HO2-immunoreactive neurons remained unaffected. |
| 1137 | 16375869 | Double-labeling studies revealed that approximately 50% of nNOS-containing neurons also contained HO2 and that the diabetes-induced change in size was confined to nNOS-immunoreactive neurons that did not contain HO2 (P < 0.01). |
| 1138 | 16375869 | No change in the size distribution occurred in neurons in which nNOS and HO2 were colocalized. |
| 1139 | 16375869 | Differences in the response of these two subpopulations of nNOS-containing neurons to diabetes could occur because they supply different targets within the gastrointestinal tract or indicate that the antioxidant, HO2, protects those nNOS-containing neurons in which it is colocalized, against oxidative stress that occurs in diabetes. |
| 1140 | 16375869 | Diabetes only affects nitric oxide synthase-containing myenteric neurons that do not contain heme oxygenase 2. |
| 1141 | 16375869 | Some of the nNOS-containing neurons also contain heme oxygenase 2 (HO2). |
| 1142 | 16375869 | Therefore, the aim of this study was to compare the effects of diabetes on HO2- and nNOS-containing neurons within the myenteric plexus of the rat ileum. |
| 1143 | 16375869 | After 12 weeks, immunostaining of wholemount preparations of ileum revealed that diabetes induced a significant shift (P < 0.001, chi-squared test for trend) towards increased neuronal cell body size in nNOS-immunoreactive neurons while HO2-immunoreactive neurons remained unaffected. |
| 1144 | 16375869 | Double-labeling studies revealed that approximately 50% of nNOS-containing neurons also contained HO2 and that the diabetes-induced change in size was confined to nNOS-immunoreactive neurons that did not contain HO2 (P < 0.01). |
| 1145 | 16375869 | No change in the size distribution occurred in neurons in which nNOS and HO2 were colocalized. |
| 1146 | 16375869 | Differences in the response of these two subpopulations of nNOS-containing neurons to diabetes could occur because they supply different targets within the gastrointestinal tract or indicate that the antioxidant, HO2, protects those nNOS-containing neurons in which it is colocalized, against oxidative stress that occurs in diabetes. |
| 1147 | 16375869 | Diabetes only affects nitric oxide synthase-containing myenteric neurons that do not contain heme oxygenase 2. |
| 1148 | 16375869 | Some of the nNOS-containing neurons also contain heme oxygenase 2 (HO2). |
| 1149 | 16375869 | Therefore, the aim of this study was to compare the effects of diabetes on HO2- and nNOS-containing neurons within the myenteric plexus of the rat ileum. |
| 1150 | 16375869 | After 12 weeks, immunostaining of wholemount preparations of ileum revealed that diabetes induced a significant shift (P < 0.001, chi-squared test for trend) towards increased neuronal cell body size in nNOS-immunoreactive neurons while HO2-immunoreactive neurons remained unaffected. |
| 1151 | 16375869 | Double-labeling studies revealed that approximately 50% of nNOS-containing neurons also contained HO2 and that the diabetes-induced change in size was confined to nNOS-immunoreactive neurons that did not contain HO2 (P < 0.01). |
| 1152 | 16375869 | No change in the size distribution occurred in neurons in which nNOS and HO2 were colocalized. |
| 1153 | 16375869 | Differences in the response of these two subpopulations of nNOS-containing neurons to diabetes could occur because they supply different targets within the gastrointestinal tract or indicate that the antioxidant, HO2, protects those nNOS-containing neurons in which it is colocalized, against oxidative stress that occurs in diabetes. |
| 1154 | 16507050 | Four pathophysiological mechanisms currently support the relationship between LUTS and erectile dysfunction (ED): (i) The nitric oxide synthase (NOS)/NO theory; there is a reduction in NOS-containing nerves in the prostate and bladder/urethra in patients with bladder outlet obstruction (BOO), and that lack of NO or loss of protein kinase G causes ED; (ii) The autonomic hyperactivity and metabolic syndrome hypothesis: benign prostatic hyperplasia (BPH) may be part of the metabolic syndrome, which includes cardiovascular diseases (e.g. hypertension, ischaemic heart disease) and diabetes mellitus, known risk factors for ED. |
| 1155 | 16507050 | The actions of several factors beside noradrenaline (e.g. endothelin-1, angiotensin II), possibly involved in the increased smooth muscle activity found in both LUTS/BPH and sexual dysfunction, are dependent on Rho-kinase activity. |
| 1156 | 16508208 | Neuronal nitric oxide synthase (nNOS) and cyclooxygenase-2 (COX-2) regulate the tubuloglomerular feedback (TGF) and renin-angiotensin system (RAS) in the kidney. |
| 1157 | 16508208 | Quantitative scores for glomerulosclerosis and interstitial fibrosis in OLETF rats were significantly higher than those of age-matched control Long-Evans Tokushima Otsuka (LETO) rats. nNOS- and COX-2-positive immunoreactions were observed in the distal tubules and collecting ducts. |
| 1158 | 16508208 | Expression of renin, angiotensin II, and inducible nitric oxide synthase (iNOS) were also examined immunohistochemically, and no differences between OLETF and LETO rats were observed in the distributions and the number of immunoreactive-sites. |
| 1159 | 16508208 | In conclusion, the overproduction of nNOS and COX-2 in the kidney of OLETF rats was confirmed, suggesting that the overproduction of nNOS and/or COX-2 does not affect the intrarenal RAS or iNOS production but does affect TGF. |
| 1160 | 16508208 | Neuronal nitric oxide synthase (nNOS) and cyclooxygenase-2 (COX-2) regulate the tubuloglomerular feedback (TGF) and renin-angiotensin system (RAS) in the kidney. |
| 1161 | 16508208 | Quantitative scores for glomerulosclerosis and interstitial fibrosis in OLETF rats were significantly higher than those of age-matched control Long-Evans Tokushima Otsuka (LETO) rats. nNOS- and COX-2-positive immunoreactions were observed in the distal tubules and collecting ducts. |
| 1162 | 16508208 | Expression of renin, angiotensin II, and inducible nitric oxide synthase (iNOS) were also examined immunohistochemically, and no differences between OLETF and LETO rats were observed in the distributions and the number of immunoreactive-sites. |
| 1163 | 16508208 | In conclusion, the overproduction of nNOS and COX-2 in the kidney of OLETF rats was confirmed, suggesting that the overproduction of nNOS and/or COX-2 does not affect the intrarenal RAS or iNOS production but does affect TGF. |
| 1164 | 16508208 | Neuronal nitric oxide synthase (nNOS) and cyclooxygenase-2 (COX-2) regulate the tubuloglomerular feedback (TGF) and renin-angiotensin system (RAS) in the kidney. |
| 1165 | 16508208 | Quantitative scores for glomerulosclerosis and interstitial fibrosis in OLETF rats were significantly higher than those of age-matched control Long-Evans Tokushima Otsuka (LETO) rats. nNOS- and COX-2-positive immunoreactions were observed in the distal tubules and collecting ducts. |
| 1166 | 16508208 | Expression of renin, angiotensin II, and inducible nitric oxide synthase (iNOS) were also examined immunohistochemically, and no differences between OLETF and LETO rats were observed in the distributions and the number of immunoreactive-sites. |
| 1167 | 16508208 | In conclusion, the overproduction of nNOS and COX-2 in the kidney of OLETF rats was confirmed, suggesting that the overproduction of nNOS and/or COX-2 does not affect the intrarenal RAS or iNOS production but does affect TGF. |
| 1168 | 16510300 | Whole kidney GFR and single nephron GFR (SNGFR) have been reported to decrease after nitric oxide synthase (NOS) inhibition. |
| 1169 | 16575507 | Macula densa nNOS is important for renin secretion, and its expression is regulated by dietary salt, renal angiotensin II, intracellular pH, and other factors. |
| 1170 | 16575507 | In salt-sensitive hypertension, nNOS is suppressed, whereas in SHR or in the early phase of diabetes, nNOS is increased in macula densa along with NADPH oxidase, which limits NO bioavailability. |
| 1171 | 16575507 | Macula densa nNOS is important for renin secretion, and its expression is regulated by dietary salt, renal angiotensin II, intracellular pH, and other factors. |
| 1172 | 16575507 | In salt-sensitive hypertension, nNOS is suppressed, whereas in SHR or in the early phase of diabetes, nNOS is increased in macula densa along with NADPH oxidase, which limits NO bioavailability. |
| 1173 | 16597606 | We investigated whether high protein induces cortical COX-2 and whether cortical COX-2 contributes to high protein-induced hyperfiltration and increased intrarenal renin biosynthesis. |
| 1174 | 16597606 | COX-2 inhibition attenuated high protein-induced hyperfiltration but had no effect on high protein-induced intrarenal renin elevation. |
| 1175 | 16597606 | Therefore, induction of cortical COX-2 contributed to high protein-induced hyperfiltration but not intrarenal renin elevation. |
| 1176 | 16597606 | In the kidney cortex, neuronal nitric oxide synthase (nNOS) is also localized to the MD, and interactions between intrarenal nNOS and COX-2 systems have been proposed. |
| 1177 | 16597606 | Cortical COX-2 elevation seen in salt restriction was blocked by nNOS inhibiton. |
| 1178 | 16597606 | Cortical nNOS expression also increased after protein loading, and inhibition of nNOS activity completely reversed high protein-induced cortical COX-2 elevation and hyperfiltration. |
| 1179 | 16597606 | These results indicate that NO is a mediator of high protein-induced cortical COX-2 elevation and suggest that both intrarenal nNOS and COX-2 systems appear to regulate afferent arteriolar tone and subsequent hyperfiltration seen in high-protein intake. |
| 1180 | 16597606 | We investigated whether high protein induces cortical COX-2 and whether cortical COX-2 contributes to high protein-induced hyperfiltration and increased intrarenal renin biosynthesis. |
| 1181 | 16597606 | COX-2 inhibition attenuated high protein-induced hyperfiltration but had no effect on high protein-induced intrarenal renin elevation. |
| 1182 | 16597606 | Therefore, induction of cortical COX-2 contributed to high protein-induced hyperfiltration but not intrarenal renin elevation. |
| 1183 | 16597606 | In the kidney cortex, neuronal nitric oxide synthase (nNOS) is also localized to the MD, and interactions between intrarenal nNOS and COX-2 systems have been proposed. |
| 1184 | 16597606 | Cortical COX-2 elevation seen in salt restriction was blocked by nNOS inhibiton. |
| 1185 | 16597606 | Cortical nNOS expression also increased after protein loading, and inhibition of nNOS activity completely reversed high protein-induced cortical COX-2 elevation and hyperfiltration. |
| 1186 | 16597606 | These results indicate that NO is a mediator of high protein-induced cortical COX-2 elevation and suggest that both intrarenal nNOS and COX-2 systems appear to regulate afferent arteriolar tone and subsequent hyperfiltration seen in high-protein intake. |
| 1187 | 16597606 | We investigated whether high protein induces cortical COX-2 and whether cortical COX-2 contributes to high protein-induced hyperfiltration and increased intrarenal renin biosynthesis. |
| 1188 | 16597606 | COX-2 inhibition attenuated high protein-induced hyperfiltration but had no effect on high protein-induced intrarenal renin elevation. |
| 1189 | 16597606 | Therefore, induction of cortical COX-2 contributed to high protein-induced hyperfiltration but not intrarenal renin elevation. |
| 1190 | 16597606 | In the kidney cortex, neuronal nitric oxide synthase (nNOS) is also localized to the MD, and interactions between intrarenal nNOS and COX-2 systems have been proposed. |
| 1191 | 16597606 | Cortical COX-2 elevation seen in salt restriction was blocked by nNOS inhibiton. |
| 1192 | 16597606 | Cortical nNOS expression also increased after protein loading, and inhibition of nNOS activity completely reversed high protein-induced cortical COX-2 elevation and hyperfiltration. |
| 1193 | 16597606 | These results indicate that NO is a mediator of high protein-induced cortical COX-2 elevation and suggest that both intrarenal nNOS and COX-2 systems appear to regulate afferent arteriolar tone and subsequent hyperfiltration seen in high-protein intake. |
| 1194 | 16597606 | We investigated whether high protein induces cortical COX-2 and whether cortical COX-2 contributes to high protein-induced hyperfiltration and increased intrarenal renin biosynthesis. |
| 1195 | 16597606 | COX-2 inhibition attenuated high protein-induced hyperfiltration but had no effect on high protein-induced intrarenal renin elevation. |
| 1196 | 16597606 | Therefore, induction of cortical COX-2 contributed to high protein-induced hyperfiltration but not intrarenal renin elevation. |
| 1197 | 16597606 | In the kidney cortex, neuronal nitric oxide synthase (nNOS) is also localized to the MD, and interactions between intrarenal nNOS and COX-2 systems have been proposed. |
| 1198 | 16597606 | Cortical COX-2 elevation seen in salt restriction was blocked by nNOS inhibiton. |
| 1199 | 16597606 | Cortical nNOS expression also increased after protein loading, and inhibition of nNOS activity completely reversed high protein-induced cortical COX-2 elevation and hyperfiltration. |
| 1200 | 16597606 | These results indicate that NO is a mediator of high protein-induced cortical COX-2 elevation and suggest that both intrarenal nNOS and COX-2 systems appear to regulate afferent arteriolar tone and subsequent hyperfiltration seen in high-protein intake. |
| 1201 | 16630608 | The inhibition of electrically induced pressor responses by 5-HT (10 microg/kg/min) in diabetic pithed rats could not be elicited after i.v. treatment with 1H-[1,2,4]Oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) (10 microg/kg), a guanylyl cyclase inhibitor, or N-omega-L-Arginine methyl ester hydrochloride (L-NAME) (10 mg/kg), a nitric oxide synthase (NOS) inhibitor. |
| 1202 | 16682803 | The parameters studied were the mesenteric arteriolar reactivity (intravital microscopy), nitric oxide synthase (NOS) activity (conversion of L-arginine to L-citrulline), eNOS gene expression (RT-PCR), NO production (diaminofluorescein), reactive oxygen species (ROS) generation (intravital fluorescence microscopy) and Cu/Zn superoxide dismutase (SOD) activity (spectrophotometry) and gene expression (RT-PCR). |
| 1203 | 16682803 | NOS activity was decreased by diabetes, but insulin did not correct it. |
| 1204 | 16682803 | However, insulin increased SOD activity but not its expression. |
| 1205 | 16682803 | In contrast to males, however, insulin does not regulate NOS in the microcirculation of diabetic females. |
| 1206 | 16682803 | The parameters studied were the mesenteric arteriolar reactivity (intravital microscopy), nitric oxide synthase (NOS) activity (conversion of L-arginine to L-citrulline), eNOS gene expression (RT-PCR), NO production (diaminofluorescein), reactive oxygen species (ROS) generation (intravital fluorescence microscopy) and Cu/Zn superoxide dismutase (SOD) activity (spectrophotometry) and gene expression (RT-PCR). |
| 1207 | 16682803 | NOS activity was decreased by diabetes, but insulin did not correct it. |
| 1208 | 16682803 | However, insulin increased SOD activity but not its expression. |
| 1209 | 16682803 | In contrast to males, however, insulin does not regulate NOS in the microcirculation of diabetic females. |
| 1210 | 16682803 | The parameters studied were the mesenteric arteriolar reactivity (intravital microscopy), nitric oxide synthase (NOS) activity (conversion of L-arginine to L-citrulline), eNOS gene expression (RT-PCR), NO production (diaminofluorescein), reactive oxygen species (ROS) generation (intravital fluorescence microscopy) and Cu/Zn superoxide dismutase (SOD) activity (spectrophotometry) and gene expression (RT-PCR). |
| 1211 | 16682803 | NOS activity was decreased by diabetes, but insulin did not correct it. |
| 1212 | 16682803 | However, insulin increased SOD activity but not its expression. |
| 1213 | 16682803 | In contrast to males, however, insulin does not regulate NOS in the microcirculation of diabetic females. |
| 1214 | 16688763 | HUVEC from gestational diabetes exhibit reduced SLC29A1 promoter activity when transfected with pGL3-hENT1(-2154) compared with pGL3-hENT1(-1114) constructs, an effect blocked by N(G)-nitro-L-arginine methyl ester (L-NAME, NOS inhibitor), but unaltered by S-nitroso-N-acetyl-L,D-penicillamine (SNAP, NO donor). |
| 1215 | 16688763 | Adenovirus-silenced eNOS expression increased hENT1 expression and activity in cells from normal or gestational diabetic pregnancies. |
| 1216 | 16741041 | Six weeks after the onset of diabetes, contractile responses to 0.1-100 nM ET-1 and relaxation responses to 1 nM-10 microM acetylcholine (ACh) in vessels preconstricted (baseline + 60%) with serotonin (5-HT) were assessed by myograph studies in the presence or absence of a nitric oxide synthase (NOS) inhibitor, N-nitro-L-arginine (L-NNA). |
| 1217 | 16741057 | This study evaluated the therapeutic potential of long-term selective blockade of the ET-1(A) receptor (ETRA) to prevent the development of retinopathy in a genetic mouse model of nonobese type 1 diabetes (NOD). |
| 1218 | 16741057 | Mice with NOD that received subcutaneous implantation of insulin pellets and wild-type control mice were treated for 4 months with the selective ETRA antagonist LU208075 (30 mg/kg/day) via drinking water. |
| 1219 | 16741057 | Retinas were removed and either fixed in formalin for confocal microscope evaluation of retinal vascular filling or transferred to RNALater for quantitative reverse transcriptase-polymerase chain reaction to evaluate expression of NOS-3, NOS-1, ET-1, ETRA, ETRB, and the angiogenic factor adrenomedullin. |
| 1220 | 16741057 | Compared with wild-type controls, expression of ET-1, ETRA, ETRB, and adrenomedullin in mice with NOD were markedly upregulated in the retinas of nontreated mice (cycle time values relative to GAPDH [deltaCt], 14.8 vs. 13.7, 18.57 vs. 17.5, 10.76 vs. 9.9, and 11.7 vs. 9.1, respectively). |
| 1221 | 16741057 | LU208075 treatment normalized the upregulated expression of ET-1 and adrenomedullin, as well as the deficit in MIFI, but did not affect the increased ETRA and ETRB expression or the elevated plasma glucose levels found in nontreated animals. |
| 1222 | 16741057 | ETRA antagonists may provide a novel therapeutic strategy to slow or prevent progression of retinal microvascular damage and proliferation in patients for whom there is clear evidence of activation of the ET-1 system. |
| 1223 | 16845211 | The results thus suggest that cognitive impairment might be due to the modulatory effect of nNOS or PDE5 enzyme on cGMP levels. |
| 1224 | 16892168 | The proposed mechanisms of erectile dysfunction (ED) in diabetic patients includes elevated advanced glycation end-products (AGEs) and increased levels of oxygen free radicals, impaired nitric oxide (NO) synthesis, increased endothelin B receptor binding sites and ultrastructural changes, upregulated RhoA/Rho-kinase pathway, NO-dependent selective nitrergic nerve degeneration and impaired cyclic guanosine monophosphate (cGMP)-dependent kinase-1 (PKG-1). |
| 1225 | 16892168 | With an appropriate vector, researchers have been able to transfect diabetic animals with agents such as neurotrophic factors and nitric oxide synthase (NOS). |
| 1226 | 16982071 | Two to three months after injection of streptozotocin, we examine in vivo responses of pial arterioles to nitric oxide synthase (NOS)-dependent (adenosine diphosphate (ADP), acetylcholine and histamine) and -independent (nitroglycerin) agonists. |
| 1227 | 16982071 | Our findings suggest that T1D impairs NOS-dependent reactivity of cerebral arterioles by a mechanism that appears to be related to the formation of superoxide via activation of PARP. |
| 1228 | 16982071 | Two to three months after injection of streptozotocin, we examine in vivo responses of pial arterioles to nitric oxide synthase (NOS)-dependent (adenosine diphosphate (ADP), acetylcholine and histamine) and -independent (nitroglycerin) agonists. |
| 1229 | 16982071 | Our findings suggest that T1D impairs NOS-dependent reactivity of cerebral arterioles by a mechanism that appears to be related to the formation of superoxide via activation of PARP. |
| 1230 | 16987713 | The aim of this study was to investigate the ability of aminoguanidine (AG) to prevent diabetes-induced changes in nitric oxide synthase- (nNOS), vasoactive intestinal polypeptide- (VIP) and noradrenaline- (NA) containing nerves of the rat ileum using immunohistochemical and biochemical techniques. |
| 1231 | 17002667 | The hsp90 inhibitor 17-allylamino-17-demethoxygeldanamycin (17-AAG; 2 x 10(-7) mol/L) or the nitric oxide synthase (NOS) inhibitor Nomega-nitro-L-arginine methyl ester (1 x 10(-5) mol/L) was added to the perfusate to observe the effects of hsp90 inhibition and hsp90-associated endothelial NOS on ischaemic responses of diabetic hearts. |
| 1232 | 17002667 | Diabetic hearts also had markedly elevated HO-1 and catalase, with no significant change in superoxide dismutase. |
| 1233 | 17031076 | NOS expression and activities were totally absent in the triply n/i/eNOS(-/-) mice before and after treatment with lipopolysaccharide. |
| 1234 | 17052961 | The association of other proteins with the nitric oxide synthase (NOS) isoforms and sGC could also serve as experimental and potentially therapeutic targets to modulate NO bioactivity. |
| 1235 | 17075048 | The NOS inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) abolished the effect of eNOS transfection. |
| 1236 | 17094672 | In the present study, increased nitric oxide synthase (NOS) enzyme activity in the aorta and decreased activity in the kidney tissue of streptozotocin-induced diabetic rats has been found in the early phase of the disease. |
| 1237 | 17130471 | Protein inhibitor of neuronal nitric oxide synthase (PIN) is a new regulator of glucose-induced insulin secretion. |
| 1238 | 17130471 | We previously showed that pancreatic beta-cells express neuronal nitric oxide synthase (nNOS) that controls insulin secretion through two catalytic activities: nitric oxide (NO) production and cytochrome c reductase activity. |
| 1239 | 17130471 | Double-immunofluorescence studies showed a colocalization of PIN with both nNOS and myosin Va in insulin-secreting beta-cells. |
| 1240 | 17130471 | Electron microscopy studies confirmed that PIN is mainly associated with insulin secretory granules and colocated with nNOS in the latter. |
| 1241 | 17130471 | In addition, PIN overexpression in INS-1 cells enhanced glucose-induced insulin secretion, which is only partly reversed by addition of an NO donor, sodium nitroprusside (SNP), and unaffected by the inhibitor of cytochrome c reductase activity, miconazole. |
| 1242 | 17130471 | In contrast, the pharmacological inhibitor of nNOS, Nomega-nitro-l-arginine methyl ester, amplified glucose-induced insulin secretion, an effect insensitive to SNP but completely normalized by the addition of miconazole. |
| 1243 | 17130471 | Thus, PIN insulinotropic effect could be related to its colocalization with the actin-based molecular motor myosin Va and as such be implicated in the physiological regulation of glucose-induced insulin secretion at the level of the exocytotic machinery. |
| 1244 | 17130471 | Protein inhibitor of neuronal nitric oxide synthase (PIN) is a new regulator of glucose-induced insulin secretion. |
| 1245 | 17130471 | We previously showed that pancreatic beta-cells express neuronal nitric oxide synthase (nNOS) that controls insulin secretion through two catalytic activities: nitric oxide (NO) production and cytochrome c reductase activity. |
| 1246 | 17130471 | Double-immunofluorescence studies showed a colocalization of PIN with both nNOS and myosin Va in insulin-secreting beta-cells. |
| 1247 | 17130471 | Electron microscopy studies confirmed that PIN is mainly associated with insulin secretory granules and colocated with nNOS in the latter. |
| 1248 | 17130471 | In addition, PIN overexpression in INS-1 cells enhanced glucose-induced insulin secretion, which is only partly reversed by addition of an NO donor, sodium nitroprusside (SNP), and unaffected by the inhibitor of cytochrome c reductase activity, miconazole. |
| 1249 | 17130471 | In contrast, the pharmacological inhibitor of nNOS, Nomega-nitro-l-arginine methyl ester, amplified glucose-induced insulin secretion, an effect insensitive to SNP but completely normalized by the addition of miconazole. |
| 1250 | 17130471 | Thus, PIN insulinotropic effect could be related to its colocalization with the actin-based molecular motor myosin Va and as such be implicated in the physiological regulation of glucose-induced insulin secretion at the level of the exocytotic machinery. |
| 1251 | 17130471 | Protein inhibitor of neuronal nitric oxide synthase (PIN) is a new regulator of glucose-induced insulin secretion. |
| 1252 | 17130471 | We previously showed that pancreatic beta-cells express neuronal nitric oxide synthase (nNOS) that controls insulin secretion through two catalytic activities: nitric oxide (NO) production and cytochrome c reductase activity. |
| 1253 | 17130471 | Double-immunofluorescence studies showed a colocalization of PIN with both nNOS and myosin Va in insulin-secreting beta-cells. |
| 1254 | 17130471 | Electron microscopy studies confirmed that PIN is mainly associated with insulin secretory granules and colocated with nNOS in the latter. |
| 1255 | 17130471 | In addition, PIN overexpression in INS-1 cells enhanced glucose-induced insulin secretion, which is only partly reversed by addition of an NO donor, sodium nitroprusside (SNP), and unaffected by the inhibitor of cytochrome c reductase activity, miconazole. |
| 1256 | 17130471 | In contrast, the pharmacological inhibitor of nNOS, Nomega-nitro-l-arginine methyl ester, amplified glucose-induced insulin secretion, an effect insensitive to SNP but completely normalized by the addition of miconazole. |
| 1257 | 17130471 | Thus, PIN insulinotropic effect could be related to its colocalization with the actin-based molecular motor myosin Va and as such be implicated in the physiological regulation of glucose-induced insulin secretion at the level of the exocytotic machinery. |
| 1258 | 17130471 | Protein inhibitor of neuronal nitric oxide synthase (PIN) is a new regulator of glucose-induced insulin secretion. |
| 1259 | 17130471 | We previously showed that pancreatic beta-cells express neuronal nitric oxide synthase (nNOS) that controls insulin secretion through two catalytic activities: nitric oxide (NO) production and cytochrome c reductase activity. |
| 1260 | 17130471 | Double-immunofluorescence studies showed a colocalization of PIN with both nNOS and myosin Va in insulin-secreting beta-cells. |
| 1261 | 17130471 | Electron microscopy studies confirmed that PIN is mainly associated with insulin secretory granules and colocated with nNOS in the latter. |
| 1262 | 17130471 | In addition, PIN overexpression in INS-1 cells enhanced glucose-induced insulin secretion, which is only partly reversed by addition of an NO donor, sodium nitroprusside (SNP), and unaffected by the inhibitor of cytochrome c reductase activity, miconazole. |
| 1263 | 17130471 | In contrast, the pharmacological inhibitor of nNOS, Nomega-nitro-l-arginine methyl ester, amplified glucose-induced insulin secretion, an effect insensitive to SNP but completely normalized by the addition of miconazole. |
| 1264 | 17130471 | Thus, PIN insulinotropic effect could be related to its colocalization with the actin-based molecular motor myosin Va and as such be implicated in the physiological regulation of glucose-induced insulin secretion at the level of the exocytotic machinery. |
| 1265 | 17146946 | NO* is produced by nitric oxide synthase (NOS) and O2*- is formed by the addition of an electron to O2 in enzymatic as well as nonenzymatic way. |
| 1266 | 17146946 | NADPH oxidase and xanthine oxidase are some of the enzymes involved in O2*- formation. |
| 1267 | 17160518 | A deficiency of gastric interstitial cells of Cajal accompanied by decreased expression of neuronal nitric oxide synthase and substance P in patients with type 2 diabetes mellitus. |
| 1268 | 17161551 | Fas (CD95) alters neuronal nitric oxide synthase expression to contribute in diabetic gastroparesis. |
| 1269 | 17170237 | Glucose, insulin, and leptin signaling pathways modulate nitric oxide synthesis in glucose-inhibited neurons in the ventromedial hypothalamus. |
| 1270 | 17170237 | Thus this study tests the hypothesis that NO synthesis is a site of convergence for glucose, leptin, and insulin signaling in VMH glucose-sensing neurons. |
| 1271 | 17170237 | With the use of the NO-sensitive dye 4-amino-5-methylamino-2',7'-difluorofluorescein in conjunction with the membrane potential-sensitive dye fluorometric imaging plate reader, we found that glucose and leptin suppress, whereas insulin stimulates neuronal nitric oxide synthase (nNOS)-dependent NO production in cultured VMH GI neurons. |
| 1272 | 17170237 | The effects of glucose and leptin were mediated by suppression of AMP-activated protein kinase (AMPK). |
| 1273 | 17170237 | The AMPK activator 5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside (AICAR) increased both NO production and neuronal activity in GI neurons. |
| 1274 | 17170237 | Furthermore, decreased glucose, insulin, and AICAR increase the phosphorylation of VMH nNOS, whereas leptin decreases it. |
| 1275 | 17170237 | Thus NO may mediate, in part, glucose, leptin, and insulin signaling in VMH glucose-sensing neurons. |
| 1276 | 17170237 | Glucose, insulin, and leptin signaling pathways modulate nitric oxide synthesis in glucose-inhibited neurons in the ventromedial hypothalamus. |
| 1277 | 17170237 | Thus this study tests the hypothesis that NO synthesis is a site of convergence for glucose, leptin, and insulin signaling in VMH glucose-sensing neurons. |
| 1278 | 17170237 | With the use of the NO-sensitive dye 4-amino-5-methylamino-2',7'-difluorofluorescein in conjunction with the membrane potential-sensitive dye fluorometric imaging plate reader, we found that glucose and leptin suppress, whereas insulin stimulates neuronal nitric oxide synthase (nNOS)-dependent NO production in cultured VMH GI neurons. |
| 1279 | 17170237 | The effects of glucose and leptin were mediated by suppression of AMP-activated protein kinase (AMPK). |
| 1280 | 17170237 | The AMPK activator 5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside (AICAR) increased both NO production and neuronal activity in GI neurons. |
| 1281 | 17170237 | Furthermore, decreased glucose, insulin, and AICAR increase the phosphorylation of VMH nNOS, whereas leptin decreases it. |
| 1282 | 17170237 | Thus NO may mediate, in part, glucose, leptin, and insulin signaling in VMH glucose-sensing neurons. |
| 1283 | 17225190 | The contractile hyporesponsiveness of the streptozotocin diabetic rat heart in vitro to beta-adrenergic agonists is eliminated when the heart is perfused with N(G)-nitro-L-arginine methyl ester (L-NAME), a non-selective inhibitor of nitric oxide synthase (NOS). |
| 1284 | 17229938 | Defective insulin and acetylcholine induction of endothelial cell-nitric oxide synthase through insulin receptor substrate/Akt signaling pathway in aorta of obese rats. |
| 1285 | 17229938 | Upon JAK2 activation, tyrosine phosphorylation of insulin receptor substrate (IRS)-1 is detected. |
| 1286 | 17229938 | In addition, ACh induces JAK2/IRS-1 and IRS-1/phosphatidylinositol (PI) 3-kinase associations, downstream activation of Akt/protein kinase B, endothelial cell-nitric oxide synthase (eNOS), and extracellular signal-regulated kinase (ERK)-1/2. |
| 1287 | 17229938 | The pharmacological blockade of JAK2 or PI 3-kinase reduced ACh-stimulated eNOS phosphorylation, NOS activity, and aorta relaxation. |
| 1288 | 17229938 | These data indicate a new signal transduction pathway for IRS-1/PI 3-kinase/Akt/eNOS activation and ERK1/2 by means of JAK2 tyrosine phosphorylation stimulated by ACh in vessels. |
| 1289 | 17229938 | Moreover, we demonstrate that in aorta of obese rats (high-fat diet), there is an impairment in the insulin- and ACh-stimulated IRS-1/PI 3-kinase pathway, leading to reduced activation with lower protein levels of eNOS associated with a hyperactivated ERK/mitogen-activated protein kinase pathway. |
| 1290 | 17229938 | These results suggest that in aorta of obese rats, there not only is insulin resistance but also ACh resistance, probably mediated by a common signaling pathway that controls the activity and the protein levels of eNOS. |
| 1291 | 17266615 | Mechanisms underlying these alterations include differential expression of equilibrative nucleoside transporters (ENTs), cationic amino acid transporters (CATs), and NOS. |
| 1292 | 17266615 | Modulation of ENTs, CATs, and NOS expression and activity in endothelium involves protein kinase C (PKC), mitogen-activated protein kinases p42 and p44 (p42/44(mapk)), calcium, and phosphatidyl inositol 3 kinase (PI3k), among others. |
| 1293 | 17266615 | However, information regarding the transcriptional modulation of ENTs, CATs, and NOS is limited. |
| 1294 | 17266615 | This review focuses on the effect of transcriptional and post-transcriptional regulatory mechanisms involved in the modulation of ENTs and CATs, and NOS expression and activity, and the consequences for foetal endothelial function in GD, IUGR and PE. |
| 1295 | 17266615 | Mechanisms underlying these alterations include differential expression of equilibrative nucleoside transporters (ENTs), cationic amino acid transporters (CATs), and NOS. |
| 1296 | 17266615 | Modulation of ENTs, CATs, and NOS expression and activity in endothelium involves protein kinase C (PKC), mitogen-activated protein kinases p42 and p44 (p42/44(mapk)), calcium, and phosphatidyl inositol 3 kinase (PI3k), among others. |
| 1297 | 17266615 | However, information regarding the transcriptional modulation of ENTs, CATs, and NOS is limited. |
| 1298 | 17266615 | This review focuses on the effect of transcriptional and post-transcriptional regulatory mechanisms involved in the modulation of ENTs and CATs, and NOS expression and activity, and the consequences for foetal endothelial function in GD, IUGR and PE. |
| 1299 | 17266615 | Mechanisms underlying these alterations include differential expression of equilibrative nucleoside transporters (ENTs), cationic amino acid transporters (CATs), and NOS. |
| 1300 | 17266615 | Modulation of ENTs, CATs, and NOS expression and activity in endothelium involves protein kinase C (PKC), mitogen-activated protein kinases p42 and p44 (p42/44(mapk)), calcium, and phosphatidyl inositol 3 kinase (PI3k), among others. |
| 1301 | 17266615 | However, information regarding the transcriptional modulation of ENTs, CATs, and NOS is limited. |
| 1302 | 17266615 | This review focuses on the effect of transcriptional and post-transcriptional regulatory mechanisms involved in the modulation of ENTs and CATs, and NOS expression and activity, and the consequences for foetal endothelial function in GD, IUGR and PE. |
| 1303 | 17266615 | Mechanisms underlying these alterations include differential expression of equilibrative nucleoside transporters (ENTs), cationic amino acid transporters (CATs), and NOS. |
| 1304 | 17266615 | Modulation of ENTs, CATs, and NOS expression and activity in endothelium involves protein kinase C (PKC), mitogen-activated protein kinases p42 and p44 (p42/44(mapk)), calcium, and phosphatidyl inositol 3 kinase (PI3k), among others. |
| 1305 | 17266615 | However, information regarding the transcriptional modulation of ENTs, CATs, and NOS is limited. |
| 1306 | 17266615 | This review focuses on the effect of transcriptional and post-transcriptional regulatory mechanisms involved in the modulation of ENTs and CATs, and NOS expression and activity, and the consequences for foetal endothelial function in GD, IUGR and PE. |
| 1307 | 17273169 | Asymmetric dimethylarginine (ADMA) and monomethyl arginine (L-NMMA) are endogenously produced amino acids that inhibit all three isoforms of nitric oxide synthase (NOS). |
| 1308 | 17323842 | Nitric oxide produced by three different isoforms of nitric oxide synthase (NOS) widely expressed in virtually all vascular cell types is mostly produced by the endothelial isoform (eNOS) in endothelial cells where it plays a crucial role in vascular tone and structure regulation. |
| 1309 | 17337232 | This molecule formed by constitutive NO synthase (NOS), endothelial (eNOS) and neuronal (nNOS), contributes to physiologically regulate ocular hemodynamics and cell viability and protects vascular endothelial cells and nerve cells or fibers against pathogenic factors associated with glaucoma, ischemia, and diabetes mellitus. |
| 1310 | 17337232 | On the other hand, NO formed by inducible NOS (iNOS) expressed under influences of inflammatory mediators evokes neurodegeneration and cell apoptosis, leading to serious ocular diseases. |
| 1311 | 17337232 | This molecule formed by constitutive NO synthase (NOS), endothelial (eNOS) and neuronal (nNOS), contributes to physiologically regulate ocular hemodynamics and cell viability and protects vascular endothelial cells and nerve cells or fibers against pathogenic factors associated with glaucoma, ischemia, and diabetes mellitus. |
| 1312 | 17337232 | On the other hand, NO formed by inducible NOS (iNOS) expressed under influences of inflammatory mediators evokes neurodegeneration and cell apoptosis, leading to serious ocular diseases. |
| 1313 | 17447001 | Four-weeks treatment decreased tissue MAO activities and caused a decrease in expression of NOS-2 and NOS-3 in heart tissue of both controls and diabetics, and a decrease of liver NOS-3 expression in controls (p < 0.05). l-Deprenyl, causing a decrease in tissue NOS expressions, might be of benefit by protecting the organism from the toxic radical effects of NO. |
| 1314 | 17596537 | Evidence for in vivo scavenging by aminoguanidine of formaldehyde produced via semicarbazide-sensitive amine oxidase-mediated deamination. |
| 1315 | 17596537 | Aminoguanidine (AG) is capable of preventing advanced protein glycation and inhibiting the activity of enzymes with carbonyl groups as cofactors, such as nitric-oxide synthase (NOS) and semicarbazide-sensitive amine oxidase (SSAO). |
| 1316 | 17596537 | Thus, AG can be an aldehyde scavenger in addition to blocking advanced glycation and inhibition of SSAO and NOS activity. |
| 1317 | 17596537 | Evidence for in vivo scavenging by aminoguanidine of formaldehyde produced via semicarbazide-sensitive amine oxidase-mediated deamination. |
| 1318 | 17596537 | Aminoguanidine (AG) is capable of preventing advanced protein glycation and inhibiting the activity of enzymes with carbonyl groups as cofactors, such as nitric-oxide synthase (NOS) and semicarbazide-sensitive amine oxidase (SSAO). |
| 1319 | 17596537 | Thus, AG can be an aldehyde scavenger in addition to blocking advanced glycation and inhibition of SSAO and NOS activity. |
| 1320 | 17647138 | Nitric oxide synthase inhibition prevents leptin induced Gn-RH release in prepubertal and peripubertal female rats. |
| 1321 | 17647138 | Since glutamate (GLU) and GABA are involved in the hypothalamic control of Gn-RH neurons and also in the neuroendocrine mechanism of puberty, in a second serie of experiments, we evaluated the effect of a competitive inhibitor of nitric oxide synthase (NOS), N-monomethyl-L-arginine (NMMA) on Gn-RH, GLU and GABA release in response to leptin. |
| 1322 | 17714081 | Aggregation responses of human platelet-rich plasma to ADP were determined in the absence or presence of 200 mg/L AGE-modified albumin (AGE-albumin), 10(-5) mol/L 17beta-oestradiol and 10(-5) mol/L ICI 182 780 (the pure oestrogen receptor antagonist). 3. |
| 1323 | 17714081 | Intraplatelet cGMP, an index of bioactive NO, was measured by radioimmunoassay and expression of nitric oxide synthase (NOS)-3, phosphoserine-1177-NOS-3 and O-glycosylated NOS-3 was quantified by western blotting in response to these same treatments. 4. |
| 1324 | 17714081 | Despite no effect on NOS-3 expression, AGE-albumin decreased and 17beta-oestradiol increased phosphoserine-1177-NOS-3 and 17beta-oestradiol largely prevented the decrease in phosphoserine-1177-NOS-3 induced by AGE-albumin. |
| 1325 | 17714081 | Alone, AGE-albumin increased O-glycosylation of NOS-3 by N-acetylglucosamine, an effect largely inhibited by 17beta-oestradiol. 5. |
| 1326 | 17714081 | In conclusion, AGE-albumin inhibits platelet NO biosynthesis through effects on serine phosphorylation and O-glycosylation of platelet NOS-3 and this may explain, at least in part, the increase in platelet aggregability induced by AGE-albumin. |
| 1327 | 17717015 | Moreover, confocal microscopy showed colocalization of insulin and pancreas duodenum homeobox-1 (PDX-1) in both endocrine and exocrine pancreas. |
| 1328 | 17717015 | This increase in insulin-expressing cells was accompanied by increased cell proliferation (observed by proliferating cell nuclear antigen-PCNA immunopositivity) which occurred in a regulated manner since it was associated with increased apoptosis (detected by the TUNEL method). |
| 1329 | 17717015 | Furthermore, L-arginine enhanced both nuclear factor-kB (NF-kB) and neuronal nitric oxide synthase (nNOS) immunopositivities. |
| 1330 | 17721990 | Co-treatment of HUVECs with 5 microM MG and 20 mM glucose significantly increased cytoplasmic free calcium levels, activation of nitric oxide synthase (NOS), caspase-3 and -9, cytochrome c release, and apoptotic cell death. |
| 1331 | 17721990 | Pretreatment with nitric oxide (NO) scavengers could inhibit 5 microM MG/20 mM glucose-induced cytochrome c release, decrease activation of caspase-9 and caspase-3, and increase the gene expression and protein levels of p53 and p21, which are known to be involved in apoptotic signaling. |
| 1332 | 17721990 | Inhibition of p53 protein expression using small interfering RNA (siRNA) blocked the activation of p21 and the cell apoptosis induced by 5 microM MG/20 mM glucose. |
| 1333 | 17721990 | In contrast, inhibition of p21 protein expression by siRNA prevented apoptosis in HUVECs but had no effect on p53 expression. |
| 1334 | 17725854 | The aim of this study was to verify the influence of improved glycaemic control with chlorpropamide on microvascular reactivity, endothelial nitric oxide synthase (e-NOS) expression, and NOS activity in neonatal streptozotocin-induced diabetic rats (n-STZ). |
| 1335 | 17827917 | The nitric oxide (NO) synthases (NOSs) system consists of three different isoforms, including neuronal (nNOS), inducible (iNOS), and endothelial NOSs (eNOS). |
| 1336 | 17827917 | NOS expression and activities were totally absent in the triply n/i/eNOS(-/-) mice before and after treatment with lipopolysaccharide. |
| 1337 | 17827917 | The nitric oxide (NO) synthases (NOSs) system consists of three different isoforms, including neuronal (nNOS), inducible (iNOS), and endothelial NOSs (eNOS). |
| 1338 | 17827917 | NOS expression and activities were totally absent in the triply n/i/eNOS(-/-) mice before and after treatment with lipopolysaccharide. |
| 1339 | 17884453 | Skeletal muscle inducible nitric oxide synthase (NOS) protein is greatly elevated in people with type 2 diabetes mellitus, whereas endothelial NOS is at normal levels. |
| 1340 | 17884453 | Diabetic rat studies suggest that skeletal muscle neuronal NOS (nNOS) micro protein expression may be reduced in human insulin resistance. |
| 1341 | 17884453 | Skeletal muscle inducible nitric oxide synthase (NOS) protein is greatly elevated in people with type 2 diabetes mellitus, whereas endothelial NOS is at normal levels. |
| 1342 | 17884453 | Diabetic rat studies suggest that skeletal muscle neuronal NOS (nNOS) micro protein expression may be reduced in human insulin resistance. |
| 1343 | 17890296 | The role of nitric oxide on matrix metalloproteinase 2 (MMP2) and MMP9 in placenta and fetus from diabetic rats. |
| 1344 | 17890296 | We found that NADPH-diaphorase activity, which reflects the distribution and activity of NO synthases (NOS), was increased in both placenta and fetuses from diabetic rats when compared with controls. |
| 1345 | 17890296 | In addition, while a NO donor enhanced MMP2 and MMP9 activities, a NOS inhibitor reduced these activities in the maternal side of the placenta from control rats. |
| 1346 | 17890296 | On the other hand, the NO donor did not modify MMP2 and MMP9 activities, while the NOS inhibitor reduced MMP9 activity in the fetal side of both control and diabetic placentas. |
| 1347 | 17890296 | The role of nitric oxide on matrix metalloproteinase 2 (MMP2) and MMP9 in placenta and fetus from diabetic rats. |
| 1348 | 17890296 | We found that NADPH-diaphorase activity, which reflects the distribution and activity of NO synthases (NOS), was increased in both placenta and fetuses from diabetic rats when compared with controls. |
| 1349 | 17890296 | In addition, while a NO donor enhanced MMP2 and MMP9 activities, a NOS inhibitor reduced these activities in the maternal side of the placenta from control rats. |
| 1350 | 17890296 | On the other hand, the NO donor did not modify MMP2 and MMP9 activities, while the NOS inhibitor reduced MMP9 activity in the fetal side of both control and diabetic placentas. |
| 1351 | 17890296 | The role of nitric oxide on matrix metalloproteinase 2 (MMP2) and MMP9 in placenta and fetus from diabetic rats. |
| 1352 | 17890296 | We found that NADPH-diaphorase activity, which reflects the distribution and activity of NO synthases (NOS), was increased in both placenta and fetuses from diabetic rats when compared with controls. |
| 1353 | 17890296 | In addition, while a NO donor enhanced MMP2 and MMP9 activities, a NOS inhibitor reduced these activities in the maternal side of the placenta from control rats. |
| 1354 | 17890296 | On the other hand, the NO donor did not modify MMP2 and MMP9 activities, while the NOS inhibitor reduced MMP9 activity in the fetal side of both control and diabetic placentas. |
| 1355 | 17989504 | We examined a possible involvement of cyclooxygenase (COX) and nitric oxide synthase (NOS) products in hyperalgesia occurring during streptozotocin (STZ)-induced diabetes. |
| 1356 | 17989504 | Indomethacin and celecoxib were used as relatively selective inhibitors of COX-1 and COX-2, respectively. |
| 1357 | 17989504 | NOS inhibitors included: non-specific inhibitor N(G)-nitro-L-arginine and L-N(6)-(1-iminoethyl)lysine preferentially acting on inducible NOS (iNOS) as well as 7-nitroindazole relatively specific inhibitor neuronal NOS (nNOS). |
| 1358 | 17989504 | The results of the study suggest participation of COX-1, COX-2 and iNOS, but not nNOS, in transmission of pain stimuli in STZ-induced diabetic hyperalgesia. |
| 1359 | 17989504 | We examined a possible involvement of cyclooxygenase (COX) and nitric oxide synthase (NOS) products in hyperalgesia occurring during streptozotocin (STZ)-induced diabetes. |
| 1360 | 17989504 | Indomethacin and celecoxib were used as relatively selective inhibitors of COX-1 and COX-2, respectively. |
| 1361 | 17989504 | NOS inhibitors included: non-specific inhibitor N(G)-nitro-L-arginine and L-N(6)-(1-iminoethyl)lysine preferentially acting on inducible NOS (iNOS) as well as 7-nitroindazole relatively specific inhibitor neuronal NOS (nNOS). |
| 1362 | 17989504 | The results of the study suggest participation of COX-1, COX-2 and iNOS, but not nNOS, in transmission of pain stimuli in STZ-induced diabetic hyperalgesia. |
| 1363 | 17989504 | We examined a possible involvement of cyclooxygenase (COX) and nitric oxide synthase (NOS) products in hyperalgesia occurring during streptozotocin (STZ)-induced diabetes. |
| 1364 | 17989504 | Indomethacin and celecoxib were used as relatively selective inhibitors of COX-1 and COX-2, respectively. |
| 1365 | 17989504 | NOS inhibitors included: non-specific inhibitor N(G)-nitro-L-arginine and L-N(6)-(1-iminoethyl)lysine preferentially acting on inducible NOS (iNOS) as well as 7-nitroindazole relatively specific inhibitor neuronal NOS (nNOS). |
| 1366 | 17989504 | The results of the study suggest participation of COX-1, COX-2 and iNOS, but not nNOS, in transmission of pain stimuli in STZ-induced diabetic hyperalgesia. |
| 1367 | 18080490 | Several parameters were evaluated: O2*- production, the levels of stable NO metabolites nitrate, nitrite and total nitrosothiols, the level of bilirubine (as marker of CO generation), inducible (iNOS) and constitutive (nNOS) mtNOS, NADH- dependent nitrate reductase (NR) and inducible arginase II (AII) activity. |
| 1368 | 18080490 | We observed that diabetes was accompanied by a significant decrease in nNOS activity, nitrite, total nitrosothiols and bilirubine content while iNOS, NR and AII activity, as well as O2*- generation was increased in heart mitochondria. |
| 1369 | 18080490 | Ecdysterone treatment normalized the levels of stable NO metabolites, ability to generate superoxide, iNOS and nNOS activity, but not bilirubine level, NR and AII activity. |
| 1370 | 18080490 | Several parameters were evaluated: O2*- production, the levels of stable NO metabolites nitrate, nitrite and total nitrosothiols, the level of bilirubine (as marker of CO generation), inducible (iNOS) and constitutive (nNOS) mtNOS, NADH- dependent nitrate reductase (NR) and inducible arginase II (AII) activity. |
| 1371 | 18080490 | We observed that diabetes was accompanied by a significant decrease in nNOS activity, nitrite, total nitrosothiols and bilirubine content while iNOS, NR and AII activity, as well as O2*- generation was increased in heart mitochondria. |
| 1372 | 18080490 | Ecdysterone treatment normalized the levels of stable NO metabolites, ability to generate superoxide, iNOS and nNOS activity, but not bilirubine level, NR and AII activity. |
| 1373 | 18080490 | Several parameters were evaluated: O2*- production, the levels of stable NO metabolites nitrate, nitrite and total nitrosothiols, the level of bilirubine (as marker of CO generation), inducible (iNOS) and constitutive (nNOS) mtNOS, NADH- dependent nitrate reductase (NR) and inducible arginase II (AII) activity. |
| 1374 | 18080490 | We observed that diabetes was accompanied by a significant decrease in nNOS activity, nitrite, total nitrosothiols and bilirubine content while iNOS, NR and AII activity, as well as O2*- generation was increased in heart mitochondria. |
| 1375 | 18080490 | Ecdysterone treatment normalized the levels of stable NO metabolites, ability to generate superoxide, iNOS and nNOS activity, but not bilirubine level, NR and AII activity. |
| 1376 | 18192221 | Oxidation of BH(4), in the setting of diabetes and other chronic vasoinflammatory conditions, can cause cofactor insufficiency and uncoupling of endothelial NOS (eNOS), manifest by a switch from nitric oxide (NO) to superoxide production. |
| 1377 | 18192221 | Since superoxide production was suppressed by NOS inhibitor treatment, eNOS was implicated as a principal superoxide source. |
| 1378 | 18192221 | Oxidation of BH(4), in the setting of diabetes and other chronic vasoinflammatory conditions, can cause cofactor insufficiency and uncoupling of endothelial NOS (eNOS), manifest by a switch from nitric oxide (NO) to superoxide production. |
| 1379 | 18192221 | Since superoxide production was suppressed by NOS inhibitor treatment, eNOS was implicated as a principal superoxide source. |
| 1380 | 18199585 | IGF-I alleviates diabetes-induced RhoA activation, eNOS uncoupling, and myocardial dysfunction. |
| 1381 | 18199585 | This study was designed to delineate the beneficial effects of IGF-I with a focus on RhoA, Akt, and eNOS coupling. |
| 1382 | 18199585 | Diabetes-induced O2(-) accumulation was ablated by the NO synthase (NOS) inhibitor nitro-L-arginine methyl ester (L-NAME), indicating endothelial NOS (eNOS) uncoupling, all of which except heart size were negated by IGF-I. |
| 1383 | 18199585 | Diabetes depressed expression of Kv1.2 and dihydrofolate reductase (DHFR), increased beta-myosin heavy-chain expression, stimulated p38 MAPK, and reduced levels of total Akt and phosphorylated Akt/eNOS, all of which with the exception of myosin heavy chain were attenuated by IGF-I. |
| 1384 | 18199585 | In addition, Y27632 and the eNOS coupler folate abrogated glucose toxicity-induced PS decline, TR90 prolongation, while it increased O2(-) and decreased NO and Kv1.2 levels. |
| 1385 | 18351463 | NO is synthesized by nitric oxide synthase (NOS) that oxidizes arginine to citrulline producing NO. |
| 1386 | 18430992 | Reduction in central insulin decreases neuronal nitric oxide synthase and increases inducible synthase activity. |
| 1387 | 18430992 | Hyperleptinemia and glucose excess, which are the other parameters of insulin resistance, may worsen the reduced astrocytic energy supply and the ongoing inflammation via the inhibition of AMP-activated protein kinase (AMPK). |
| 1388 | 18465682 | We investigate muscle fiber composition, fiber-specific glycolytic and oxidative enzyme capacity and nitric oxide synthase (NOS) expression in skeletal muscle of patients with type 1 diabetes (T1D) compared to individuals with normal glucose tolerance (NGT). |
| 1389 | 18497878 | Vasoinhibins prevent retinal vasopermeability associated with diabetic retinopathy in rats via protein phosphatase 2A-dependent eNOS inactivation. |
| 1390 | 18497878 | Vasoinhibins, a family of peptides derived from the protein hormone prolactin (and inclusive of the 16-kDa fragment of prolactin), antagonize the proangiogenic effects of VEGF, a primary mediator of retinal vasopermeability. |
| 1391 | 18497878 | Inhibition by vasoinhibins was similar to that achieved following immunodepletion of VEGF from human diabetic retinopathy vitreous or blockage of NO synthesis, suggesting that vasoinhibins inhibit VEGF-induced NOS activation. |
| 1392 | 18497878 | We further showed that vasoinhibins activate protein phosphatase 2A (PP2A), leading to eNOS dephosphorylation at Ser1179 and, thereby, eNOS inactivation. |
| 1393 | 18519240 | Nitric oxide (NO) is produced by NO synthase (NOS) isoforms: neuronal NOS (nNOS), endothelial NOS (eNOS) and inducible NOS (iNOS). |
| 1394 | 18519240 | It is believed that, while nNOS and eNOS are effective in regulation of normal physiological processes, iNOS is expressed at an increasing rate especially in inflammatory process. |
| 1395 | 18519240 | Nitric oxide (NO) is produced by NO synthase (NOS) isoforms: neuronal NOS (nNOS), endothelial NOS (eNOS) and inducible NOS (iNOS). |
| 1396 | 18519240 | It is believed that, while nNOS and eNOS are effective in regulation of normal physiological processes, iNOS is expressed at an increasing rate especially in inflammatory process. |
| 1397 | 18596108 | In this double-blind study, 48 healthy volunteers were randomized to GLP-1-(7-36) amide, the nitric oxide synthase (NOS) inhibitor N(G)-monomethyl-l-arginine acetate (l-NMMA), the alpha(2)-adrenergic antagonist yohimbine, or placebo (i.e., saline), alone or in combination. |
| 1398 | 18607348 | An elevation of podocyte VEGF expression correlated with infiltration of Flt-1-positive macrophage in injured glomeruli in diabetic eNOS KO mice, suggesting that VEGF could contribute to macrophage migration. |
| 1399 | 18607348 | Neither renal nNOS nor iNOS expression was altered in both C57BL/6 and eNOS KO mice. |
| 1400 | 18692595 | Nitric oxide (NO) is a gaseous lipophilic free radical generated by three distinct isoforms of nitric oxide synthases (NOS), type 1 or neuronal (nNOS), type 2 or inducible (iNOS) and type 3 or endothelial NOS (eNOS). |
| 1401 | 18692595 | Here we review the transcriptional regulation of endothelial NOS and factors affecting eNOS activity and function, as well as the important vascular pathologies associated with altered NOS function, focusing on the regulatory role of hsp90 and other factors in NO-associated pathogenesis of these diseases. |
| 1402 | 18692595 | Nitric oxide (NO) is a gaseous lipophilic free radical generated by three distinct isoforms of nitric oxide synthases (NOS), type 1 or neuronal (nNOS), type 2 or inducible (iNOS) and type 3 or endothelial NOS (eNOS). |
| 1403 | 18692595 | Here we review the transcriptional regulation of endothelial NOS and factors affecting eNOS activity and function, as well as the important vascular pathologies associated with altered NOS function, focusing on the regulatory role of hsp90 and other factors in NO-associated pathogenesis of these diseases. |
| 1404 | 18810243 | The effect of CB-1 and CB-2 receptor agonists, as well as an influence of a non-selective inhibitor of nitric oxide synthase (NOS), L-NOArg, and an inhibitor acting preferentially on cyclooxygenase-1 (COX-1), indomethacin, on the action of cannabinoid receptor agonists in a streptozotocin (STZ)-induced neuropathic model was investigated. |
| 1405 | 18810243 | When administered alone, a non-selective cannabinoid receptor agonist, WIN 55,212-2, a potentially selective CB-1 cannabinoid receptor agonist, Met-F-AEA, and a selective CB-2 cannabinoid receptor agonist, AM1241, dose-dependently reduced STZ-induced hyperalgesia. |
| 1406 | 18810243 | The results of the present study also demonstrated that inhibitors of COX and NOS increase antihyperalgesic activity of low doses of CB-1 and CB-2 receptor agonists. |
| 1407 | 18810243 | The effect of CB-1 and CB-2 receptor agonists, as well as an influence of a non-selective inhibitor of nitric oxide synthase (NOS), L-NOArg, and an inhibitor acting preferentially on cyclooxygenase-1 (COX-1), indomethacin, on the action of cannabinoid receptor agonists in a streptozotocin (STZ)-induced neuropathic model was investigated. |
| 1408 | 18810243 | When administered alone, a non-selective cannabinoid receptor agonist, WIN 55,212-2, a potentially selective CB-1 cannabinoid receptor agonist, Met-F-AEA, and a selective CB-2 cannabinoid receptor agonist, AM1241, dose-dependently reduced STZ-induced hyperalgesia. |
| 1409 | 18810243 | The results of the present study also demonstrated that inhibitors of COX and NOS increase antihyperalgesic activity of low doses of CB-1 and CB-2 receptor agonists. |
| 1410 | 18924487 | Then, both reactive species are produced by strictly regulated enzymes, such as nitric oxide synthase (NOS), and isoforms of NADPH oxidase, or as by-products from not so well regulated sources, such as the mitochondrial electron-transport chain. |
| 1411 | 18931023 | We tested the hypothesis that 17beta-estradiol (E(2)) has dual effects on the heart, increasing levels of proteins thought to have beneficial cardiovascular effects (e.g. endothelial nitric oxide (NO) synthase (eNOS)) as well as those thought to have detrimental cardiovascular effects (e.g. type 1 angiotensin II (AngII) receptor (AT(1)R)). |
| 1412 | 18931023 | Ovariectomized Wistar rats consuming a high-sodium diet received one of four treatments (n=7 per group): group 1, placebo pellets; group 2, E(2) (0 x 5 mg/pellet, 21-day release); group 3, NOS inhibitor, N(omega)-nitro-L-arginine-methyl-ester (L-NAME; 40 mg/kg per day for 14 days) plus Ang II (0 x 225 mg/kg per day on days 11-14); group 4, E(2) plus L-NAME/Ang II. |
| 1413 | 18931023 | E(2) increased cardiac levels of estrogen receptors ESR1 and ESR2, an ESR-associated membrane protein caveolin-3, eNOS, and phosphorylated (p)eNOS, thus, exerting potentially beneficial cardiovascular effects on NO. |
| 1414 | 18931023 | However, E(2) also increased cardiac levels of proteins associated with cardiovascular injury and inflammation including, AT(1)R, protein kinase C delta (PRKCD), phosphorylated PRKC, and phosphorylated extracellular signal regulated kinase (pMAPK)3/1, plasminogen activator inhibitor-1 (PAI-1), osteopontin and ED-1, a monocyte/macrophage-specific protein. |
| 1415 | 18931023 | E(2) treatment led to similar protein changes in the hearts of L-NAME/Ang II-treated rats except that the increase in peNOS was prevented, and L-NAME/Ang II and E(2) had additive effects in increasing cardiac PRKCD and PAI-1. |
| 1416 | 18931023 | Thus, the highest levels of cardiac PAI-1 and PRKCD occurred in L-NAME/Ang II-treated rats receiving E(2). |
| 1417 | 18953659 | Vitamin E supplementation in rats with experimental diabetes mellitus: analysis of myosin-V and nNOS immunoreactive myenteric neurons from terminal ileum. |
| 1418 | 18953659 | The effect of vitamin E (1 g/kg body weight) supplementation on myosin-V and neuronal nitric oxide synthase (nNOS) immunoreactive myenteric neurons from the ileum of diabetic rats was investigated in the present study. |
| 1419 | 18953659 | Myosin-V and nNOS immunoreactive neuronal cell body area increased significantly in group NE. |
| 1420 | 18953659 | The area of myosin-V and nNOS myenteric neurons also increased in group D. |
| 1421 | 18953659 | Vitamin E supplementation in rats with experimental diabetes mellitus: analysis of myosin-V and nNOS immunoreactive myenteric neurons from terminal ileum. |
| 1422 | 18953659 | The effect of vitamin E (1 g/kg body weight) supplementation on myosin-V and neuronal nitric oxide synthase (nNOS) immunoreactive myenteric neurons from the ileum of diabetic rats was investigated in the present study. |
| 1423 | 18953659 | Myosin-V and nNOS immunoreactive neuronal cell body area increased significantly in group NE. |
| 1424 | 18953659 | The area of myosin-V and nNOS myenteric neurons also increased in group D. |
| 1425 | 18953659 | Vitamin E supplementation in rats with experimental diabetes mellitus: analysis of myosin-V and nNOS immunoreactive myenteric neurons from terminal ileum. |
| 1426 | 18953659 | The effect of vitamin E (1 g/kg body weight) supplementation on myosin-V and neuronal nitric oxide synthase (nNOS) immunoreactive myenteric neurons from the ileum of diabetic rats was investigated in the present study. |
| 1427 | 18953659 | Myosin-V and nNOS immunoreactive neuronal cell body area increased significantly in group NE. |
| 1428 | 18953659 | The area of myosin-V and nNOS myenteric neurons also increased in group D. |
| 1429 | 18953659 | Vitamin E supplementation in rats with experimental diabetes mellitus: analysis of myosin-V and nNOS immunoreactive myenteric neurons from terminal ileum. |
| 1430 | 18953659 | The effect of vitamin E (1 g/kg body weight) supplementation on myosin-V and neuronal nitric oxide synthase (nNOS) immunoreactive myenteric neurons from the ileum of diabetic rats was investigated in the present study. |
| 1431 | 18953659 | Myosin-V and nNOS immunoreactive neuronal cell body area increased significantly in group NE. |
| 1432 | 18953659 | The area of myosin-V and nNOS myenteric neurons also increased in group D. |
| 1433 | 19041728 | Diabetic subjects exhibit low levels of nitric oxide (NO), its precursor L-arginine, and nitric oxide synthase (NOS) in tissues like endothelium and kidney. |
| 1434 | 19094928 | Peroxisome proliferators activated receptors (PPAR) are ligand-inducible nuclear transacting factors comprising three subtypes, PPARalpha, PPARbeta/delta and PPARgamma, which play a key role in lipids and glucose homeostasis. |
| 1435 | 19094928 | All PPAR subtypes have been identified in joint or inflammatory cells and their activation resulted in a transcriptional repression of pro-inflammatory cytokines (IL-1, TNFalpha), early inflammatory genes (NOS(2), COX-2, mPGES-1) or matrix metalloproteases (MMP-1, MMP-13), at least for the gamma subtype. |
| 1436 | 19094928 | PPAR full agonists were also shown to stimulate IL-1 receptor antagonist (IL-1Ra) production by cytokine-stimulated articular cells in a subtype-dependent manner. |
| 1437 | 19094928 | These anti-inflammatory and anti-catabolic properties were confirmed in animal models of joint diseases where PPAR agonists reduced synovial inflammation while preventing cartilage destruction or inflammatory bone loss, although many effects required much higher doses than needed to restore insulin sensitivity or to lower circulating lipid levels. |
| 1438 | 19094928 | However, these promising effects of PPAR full agonists were hampered by their ability to reduce the growth factor-dependent synthesis of extracellular matrix components or to induce chondrocyte apoptosis, by the possible contribution of immunosuppressive properties to their anti-arthritic effects, by the increased adipocyte differentiation secondary to prolonged stimulation of PPARgamma, and by a variable contribution of PPAR subtypes depending on the system. |
| 1439 | 19140154 | In order to clarify the mechanism of aucubin's neuroprotection, the activities of endogenous antioxidants and nitric oxide synthase (NOS) together with the content of lipid peroxide in the hippocampus were assayed. |
| 1440 | 19273327 | Alterations contributing to oxidative and nitrosative stress, including elevated nitric oxide (NO) and superoxide production, overexpression of different isoforms of nitric oxide synthase (NOS), nitrated and poly(ADP-ribosy)lated proteins, and downregulation of antioxidative enzymes have been implicated in the pathogenesis of this ocular disease. |
| 1441 | 19286954 | Antidiabetic drug pioglitazone protects the heart via activation of PPAR-gamma receptors, PI3-kinase, Akt, and eNOS pathway in a rabbit model of myocardial infarction. |
| 1442 | 19286954 | Rabbits were assigned randomly to nine groups (n = 10 in each): the control group (fed a normal diet), pioglitazone group (fed diets containing 1 mg.kg(-1).day(-1) pioglitazone), pioglitazone + 5-hydroxydecanoic acid (HD) group [fed the pioglitazone diet + 5 mg/kg iv 5-HD, a mitochondrial ATP-sensitive K(+) (K(ATP)) channel blocker], pioglitazone + GW9662 group [fed the pioglitazone diet + 2 mg/kg iv GW9662, a peroxisome proliferator activated receptor (PPAR)-gamma antagonist], GW9662 group (fed a normal diet + iv GW9662), pioglitazone + wortmannin group [fed the pioglitazone diet + 0.6 mg/kg iv wortmannin, a phosphatidylinositol (PI)3-kinase inhibitor], wortmannin group (fed a normal diet + iv wortmannin), pioglitazone + nitro-l-arginine methyl ester (l-NAME) group [fed the pioglitazone diet + 10 mg/kg iv l-NAME, a nitric oxide synthase (NOS) inhibitor], and l-NAME group (fed a normal diet + iv l-NAME). |
| 1443 | 19286954 | Western blotting was performed to assess levels of Akt and phospho-Akt and phospho-endothelial NOS (eNOS) in the myocardium following reperfusion. |
| 1444 | 19286954 | Pioglitazone reduces the myocardial infarct size via activation of PPAR-gamma, PI3-kinase, Akt, and eNOS pathways, but not via opening the mitochondrial K(ATP) channel. |
| 1445 | 19286954 | Antidiabetic drug pioglitazone protects the heart via activation of PPAR-gamma receptors, PI3-kinase, Akt, and eNOS pathway in a rabbit model of myocardial infarction. |
| 1446 | 19286954 | Rabbits were assigned randomly to nine groups (n = 10 in each): the control group (fed a normal diet), pioglitazone group (fed diets containing 1 mg.kg(-1).day(-1) pioglitazone), pioglitazone + 5-hydroxydecanoic acid (HD) group [fed the pioglitazone diet + 5 mg/kg iv 5-HD, a mitochondrial ATP-sensitive K(+) (K(ATP)) channel blocker], pioglitazone + GW9662 group [fed the pioglitazone diet + 2 mg/kg iv GW9662, a peroxisome proliferator activated receptor (PPAR)-gamma antagonist], GW9662 group (fed a normal diet + iv GW9662), pioglitazone + wortmannin group [fed the pioglitazone diet + 0.6 mg/kg iv wortmannin, a phosphatidylinositol (PI)3-kinase inhibitor], wortmannin group (fed a normal diet + iv wortmannin), pioglitazone + nitro-l-arginine methyl ester (l-NAME) group [fed the pioglitazone diet + 10 mg/kg iv l-NAME, a nitric oxide synthase (NOS) inhibitor], and l-NAME group (fed a normal diet + iv l-NAME). |
| 1447 | 19286954 | Western blotting was performed to assess levels of Akt and phospho-Akt and phospho-endothelial NOS (eNOS) in the myocardium following reperfusion. |
| 1448 | 19286954 | Pioglitazone reduces the myocardial infarct size via activation of PPAR-gamma, PI3-kinase, Akt, and eNOS pathways, but not via opening the mitochondrial K(ATP) channel. |
| 1449 | 19458119 | The mTAL expresses all three isoforms of nitric oxide synthase (NOS), which are subject to phosphoregulation and represent substrates for PP2B. |
| 1450 | 19458119 | Analysis of specific NOS isoform activity revealed increased NOS1 and NOS2 activities in mTALs from STZ rats. |
| 1451 | 19458119 | Western blot analysis detected no differences in NOS isoform expression, although phosphorylation of pThr(495)-NOS3 was significantly reduced in mTALs from STZ rats. |
| 1452 | 19458119 | Phosphorylation of pSer(852)-NOS1, pSer(633)-NOS3, and pSer(1177)-NOS3 was similar in mTALs from STZ and sham rats. |
| 1453 | 19458119 | Inhibition of PP2B did not alter the phosphorylation of NOS1 or NOS3 at known sites. |
| 1454 | 19458119 | In conclusion, while NO bioavailability in mTALs is reduced during diabetes, free radical scavenging with tempol unmasks increased NO production that involves PP2B-dependent activation of NOS1 and NOS2. |
| 1455 | 19458119 | The mTAL expresses all three isoforms of nitric oxide synthase (NOS), which are subject to phosphoregulation and represent substrates for PP2B. |
| 1456 | 19458119 | Analysis of specific NOS isoform activity revealed increased NOS1 and NOS2 activities in mTALs from STZ rats. |
| 1457 | 19458119 | Western blot analysis detected no differences in NOS isoform expression, although phosphorylation of pThr(495)-NOS3 was significantly reduced in mTALs from STZ rats. |
| 1458 | 19458119 | Phosphorylation of pSer(852)-NOS1, pSer(633)-NOS3, and pSer(1177)-NOS3 was similar in mTALs from STZ and sham rats. |
| 1459 | 19458119 | Inhibition of PP2B did not alter the phosphorylation of NOS1 or NOS3 at known sites. |
| 1460 | 19458119 | In conclusion, while NO bioavailability in mTALs is reduced during diabetes, free radical scavenging with tempol unmasks increased NO production that involves PP2B-dependent activation of NOS1 and NOS2. |
| 1461 | 19458119 | The mTAL expresses all three isoforms of nitric oxide synthase (NOS), which are subject to phosphoregulation and represent substrates for PP2B. |
| 1462 | 19458119 | Analysis of specific NOS isoform activity revealed increased NOS1 and NOS2 activities in mTALs from STZ rats. |
| 1463 | 19458119 | Western blot analysis detected no differences in NOS isoform expression, although phosphorylation of pThr(495)-NOS3 was significantly reduced in mTALs from STZ rats. |
| 1464 | 19458119 | Phosphorylation of pSer(852)-NOS1, pSer(633)-NOS3, and pSer(1177)-NOS3 was similar in mTALs from STZ and sham rats. |
| 1465 | 19458119 | Inhibition of PP2B did not alter the phosphorylation of NOS1 or NOS3 at known sites. |
| 1466 | 19458119 | In conclusion, while NO bioavailability in mTALs is reduced during diabetes, free radical scavenging with tempol unmasks increased NO production that involves PP2B-dependent activation of NOS1 and NOS2. |
| 1467 | 19458119 | The mTAL expresses all three isoforms of nitric oxide synthase (NOS), which are subject to phosphoregulation and represent substrates for PP2B. |
| 1468 | 19458119 | Analysis of specific NOS isoform activity revealed increased NOS1 and NOS2 activities in mTALs from STZ rats. |
| 1469 | 19458119 | Western blot analysis detected no differences in NOS isoform expression, although phosphorylation of pThr(495)-NOS3 was significantly reduced in mTALs from STZ rats. |
| 1470 | 19458119 | Phosphorylation of pSer(852)-NOS1, pSer(633)-NOS3, and pSer(1177)-NOS3 was similar in mTALs from STZ and sham rats. |
| 1471 | 19458119 | Inhibition of PP2B did not alter the phosphorylation of NOS1 or NOS3 at known sites. |
| 1472 | 19458119 | In conclusion, while NO bioavailability in mTALs is reduced during diabetes, free radical scavenging with tempol unmasks increased NO production that involves PP2B-dependent activation of NOS1 and NOS2. |
| 1473 | 19458119 | The mTAL expresses all three isoforms of nitric oxide synthase (NOS), which are subject to phosphoregulation and represent substrates for PP2B. |
| 1474 | 19458119 | Analysis of specific NOS isoform activity revealed increased NOS1 and NOS2 activities in mTALs from STZ rats. |
| 1475 | 19458119 | Western blot analysis detected no differences in NOS isoform expression, although phosphorylation of pThr(495)-NOS3 was significantly reduced in mTALs from STZ rats. |
| 1476 | 19458119 | Phosphorylation of pSer(852)-NOS1, pSer(633)-NOS3, and pSer(1177)-NOS3 was similar in mTALs from STZ and sham rats. |
| 1477 | 19458119 | Inhibition of PP2B did not alter the phosphorylation of NOS1 or NOS3 at known sites. |
| 1478 | 19458119 | In conclusion, while NO bioavailability in mTALs is reduced during diabetes, free radical scavenging with tempol unmasks increased NO production that involves PP2B-dependent activation of NOS1 and NOS2. |
| 1479 | 19458119 | The mTAL expresses all three isoforms of nitric oxide synthase (NOS), which are subject to phosphoregulation and represent substrates for PP2B. |
| 1480 | 19458119 | Analysis of specific NOS isoform activity revealed increased NOS1 and NOS2 activities in mTALs from STZ rats. |
| 1481 | 19458119 | Western blot analysis detected no differences in NOS isoform expression, although phosphorylation of pThr(495)-NOS3 was significantly reduced in mTALs from STZ rats. |
| 1482 | 19458119 | Phosphorylation of pSer(852)-NOS1, pSer(633)-NOS3, and pSer(1177)-NOS3 was similar in mTALs from STZ and sham rats. |
| 1483 | 19458119 | Inhibition of PP2B did not alter the phosphorylation of NOS1 or NOS3 at known sites. |
| 1484 | 19458119 | In conclusion, while NO bioavailability in mTALs is reduced during diabetes, free radical scavenging with tempol unmasks increased NO production that involves PP2B-dependent activation of NOS1 and NOS2. |
| 1485 | 19465935 | Although the ICP/MAP ratio and the expression levels of endothelial NOS (eNOS) and neuronal NOS (nNOS) in the CC were markedly decreased in diabetic rats, long-term udenafil treatment improved the erectile function and increased cNOS expression compared with diabetic controls. |
| 1486 | 19485884 | Modulation of ENTs and NOS expression and activity in endothelium involves several signalling molecules, including protein kinase C, mitogen-activated protein kinases p42 and p44, calcium and phosphatidyl inositol 3 kinase. |
| 1487 | 19531636 | Although cutaneous SHH and Patched-1 (Ptc-1 encoded by PTCH, PTCH 1) proteins were increased significantly on day 4 after wounding compared with day 0 in normal mice, both were decreased significantly in STZ-induced diabetic mice. |
| 1488 | 19531636 | Topical application of SHH restored wound healing delay in STZ-induced diabetic mice, with a concomitant augmentation of both cutaneous constitutive nitric oxide synthase (NOS) activity and nitrite level. |
| 1489 | 19531636 | After 24-h treatment in vitro, SHH (5-20 microg/ml) significantly increased cutaneous endothelial NOS protein expression, NOS activity and NO level in normal mice and STZ-induced diabetic mice in a concentration-dependent manner, an effect that was blunted by cyclopamine and NOS inhibitor N(omega)-nitro-L-arginine methyl ester. |
| 1490 | 19531636 | The phosphatidylinositol 3-kinase inhibitor LY-294002 significantly blunted the increase of NOS activity and NO level induced by SHH treatment in human umbilican vein endothelial cells. |
| 1491 | 19531636 | Although cutaneous SHH and Patched-1 (Ptc-1 encoded by PTCH, PTCH 1) proteins were increased significantly on day 4 after wounding compared with day 0 in normal mice, both were decreased significantly in STZ-induced diabetic mice. |
| 1492 | 19531636 | Topical application of SHH restored wound healing delay in STZ-induced diabetic mice, with a concomitant augmentation of both cutaneous constitutive nitric oxide synthase (NOS) activity and nitrite level. |
| 1493 | 19531636 | After 24-h treatment in vitro, SHH (5-20 microg/ml) significantly increased cutaneous endothelial NOS protein expression, NOS activity and NO level in normal mice and STZ-induced diabetic mice in a concentration-dependent manner, an effect that was blunted by cyclopamine and NOS inhibitor N(omega)-nitro-L-arginine methyl ester. |
| 1494 | 19531636 | The phosphatidylinositol 3-kinase inhibitor LY-294002 significantly blunted the increase of NOS activity and NO level induced by SHH treatment in human umbilican vein endothelial cells. |
| 1495 | 19531636 | Although cutaneous SHH and Patched-1 (Ptc-1 encoded by PTCH, PTCH 1) proteins were increased significantly on day 4 after wounding compared with day 0 in normal mice, both were decreased significantly in STZ-induced diabetic mice. |
| 1496 | 19531636 | Topical application of SHH restored wound healing delay in STZ-induced diabetic mice, with a concomitant augmentation of both cutaneous constitutive nitric oxide synthase (NOS) activity and nitrite level. |
| 1497 | 19531636 | After 24-h treatment in vitro, SHH (5-20 microg/ml) significantly increased cutaneous endothelial NOS protein expression, NOS activity and NO level in normal mice and STZ-induced diabetic mice in a concentration-dependent manner, an effect that was blunted by cyclopamine and NOS inhibitor N(omega)-nitro-L-arginine methyl ester. |
| 1498 | 19531636 | The phosphatidylinositol 3-kinase inhibitor LY-294002 significantly blunted the increase of NOS activity and NO level induced by SHH treatment in human umbilican vein endothelial cells. |
| 1499 | 19543853 | We performed organ bath studies, and examined the changes in expression levels of muscarinic M(3) receptor, endothelial, inducible, and neuronal nitric oxide synthase (eNOS, iNOS, and nNOS, respectively) mRNAs in the rat aorta utilizing real-time polymerase chain reaction in 12-week-old and 70-week-old GK rats as well as in age-matched Wistar rats. |
| 1500 | 19543853 | In the 12-week-old GK rat aorta, a significant increase in norepinephrine-induced contraction and a significant decrease in acetylcholine-induced relaxation as well as significant increases in expression levels of muscarinic M(3) receptor and eNOS and a significant decrease in nNOS mRNAs were observed compared to age-matched controls. |
| 1501 | 19543853 | In the older GK rat aorta, significant decreases in acetylcholine- and nitroglycerine-induced relaxations as well as significant decreases in the expression levels of muscarinic M(3) receptor, eNOS, iNOS, and nNOS mRNAs were observed compared to those in the younger GK rats. |
| 1502 | 19543853 | In contrast, although significant decreases in acetylcholine and nitroglycerine-induced relaxations were observed, the expression levels of muscarinic M(3) receptor, eNOS, iNOS, and nNOS mRNAs in the older Wistar rats aorta were unchanged, increased, increased and decreased, respectively, compared to the younger Wistar rat aorta. |
| 1503 | 19543853 | We performed organ bath studies, and examined the changes in expression levels of muscarinic M(3) receptor, endothelial, inducible, and neuronal nitric oxide synthase (eNOS, iNOS, and nNOS, respectively) mRNAs in the rat aorta utilizing real-time polymerase chain reaction in 12-week-old and 70-week-old GK rats as well as in age-matched Wistar rats. |
| 1504 | 19543853 | In the 12-week-old GK rat aorta, a significant increase in norepinephrine-induced contraction and a significant decrease in acetylcholine-induced relaxation as well as significant increases in expression levels of muscarinic M(3) receptor and eNOS and a significant decrease in nNOS mRNAs were observed compared to age-matched controls. |
| 1505 | 19543853 | In the older GK rat aorta, significant decreases in acetylcholine- and nitroglycerine-induced relaxations as well as significant decreases in the expression levels of muscarinic M(3) receptor, eNOS, iNOS, and nNOS mRNAs were observed compared to those in the younger GK rats. |
| 1506 | 19543853 | In contrast, although significant decreases in acetylcholine and nitroglycerine-induced relaxations were observed, the expression levels of muscarinic M(3) receptor, eNOS, iNOS, and nNOS mRNAs in the older Wistar rats aorta were unchanged, increased, increased and decreased, respectively, compared to the younger Wistar rat aorta. |
| 1507 | 19543853 | We performed organ bath studies, and examined the changes in expression levels of muscarinic M(3) receptor, endothelial, inducible, and neuronal nitric oxide synthase (eNOS, iNOS, and nNOS, respectively) mRNAs in the rat aorta utilizing real-time polymerase chain reaction in 12-week-old and 70-week-old GK rats as well as in age-matched Wistar rats. |
| 1508 | 19543853 | In the 12-week-old GK rat aorta, a significant increase in norepinephrine-induced contraction and a significant decrease in acetylcholine-induced relaxation as well as significant increases in expression levels of muscarinic M(3) receptor and eNOS and a significant decrease in nNOS mRNAs were observed compared to age-matched controls. |
| 1509 | 19543853 | In the older GK rat aorta, significant decreases in acetylcholine- and nitroglycerine-induced relaxations as well as significant decreases in the expression levels of muscarinic M(3) receptor, eNOS, iNOS, and nNOS mRNAs were observed compared to those in the younger GK rats. |
| 1510 | 19543853 | In contrast, although significant decreases in acetylcholine and nitroglycerine-induced relaxations were observed, the expression levels of muscarinic M(3) receptor, eNOS, iNOS, and nNOS mRNAs in the older Wistar rats aorta were unchanged, increased, increased and decreased, respectively, compared to the younger Wistar rat aorta. |
| 1511 | 19543853 | We performed organ bath studies, and examined the changes in expression levels of muscarinic M(3) receptor, endothelial, inducible, and neuronal nitric oxide synthase (eNOS, iNOS, and nNOS, respectively) mRNAs in the rat aorta utilizing real-time polymerase chain reaction in 12-week-old and 70-week-old GK rats as well as in age-matched Wistar rats. |
| 1512 | 19543853 | In the 12-week-old GK rat aorta, a significant increase in norepinephrine-induced contraction and a significant decrease in acetylcholine-induced relaxation as well as significant increases in expression levels of muscarinic M(3) receptor and eNOS and a significant decrease in nNOS mRNAs were observed compared to age-matched controls. |
| 1513 | 19543853 | In the older GK rat aorta, significant decreases in acetylcholine- and nitroglycerine-induced relaxations as well as significant decreases in the expression levels of muscarinic M(3) receptor, eNOS, iNOS, and nNOS mRNAs were observed compared to those in the younger GK rats. |
| 1514 | 19543853 | In contrast, although significant decreases in acetylcholine and nitroglycerine-induced relaxations were observed, the expression levels of muscarinic M(3) receptor, eNOS, iNOS, and nNOS mRNAs in the older Wistar rats aorta were unchanged, increased, increased and decreased, respectively, compared to the younger Wistar rat aorta. |
| 1515 | 19578741 | Aminoguanidine, as an example, is an anti-oxidant, a nitric oxide synthase inhibitor (NOS) which prevents nitric oxide formation, and an inhibitor of advanced glycosylation end products (AGEs). |
| 1516 | 19649339 | The aim of this study was to examine the effects of leptin on aortic rings with and without endothelium isolated from streptozotocin (STZ)-induced diabetic and control rats, and also in the presence of an inhibitor of nitric oxide synthase (NOS). |
| 1517 | 19717727 | Activation of the PDK-1/Akt/eNOS pathway involved in aortic endothelial function differs between hyperinsulinemic and insulin-deficient diabetic rats. |
| 1518 | 19717727 | In diabetic states, altered plasma insulin is likely to play key roles in 3-phosphoinositide-dependent protein kinase (PDK)/Akt pathway activation, in insulin resistance and in endothelial dysfunction. |
| 1519 | 19717727 | Since the molecular mechanism(s) remains unclear, we examined the relationship between the PDK/Akt/endothelial nitric oxide synthase (NOS) pathway and endothelial function in aortas from diabetic rats that were either insulin deficient or hyperinsulinemic. |
| 1520 | 19717727 | The insulin-induced relaxation was inhibited by treatment with an Akt inhibitor in control and diabetic aortas, but not in the HI-diabetic aorta. |
| 1521 | 19717727 | In the diabetic group, various insulin-stimulated levels (nitric oxide production, phosphorylation of endothelial NOS at Ser(1177), of Akt at Thr(308), and of PDK-1 at Ser(241)) were significantly increased, whereas, in the HI-diabetic group, these levels were all decreased (vs. control aortas). |
| 1522 | 19717727 | These results suggest that the plasma insulin level has a close relation to the level of aortic PDK-1/Akt (at Thr(308))/NOS activities, and that reduced actions of the PDK-1/Akt (at Thr(308)) signal pathway may contribute to the impairments of insulin-induced endothelial functions seen in hyperinsulinemic diabetes. |
| 1523 | 19717727 | Activation of the PDK-1/Akt/eNOS pathway involved in aortic endothelial function differs between hyperinsulinemic and insulin-deficient diabetic rats. |
| 1524 | 19717727 | In diabetic states, altered plasma insulin is likely to play key roles in 3-phosphoinositide-dependent protein kinase (PDK)/Akt pathway activation, in insulin resistance and in endothelial dysfunction. |
| 1525 | 19717727 | Since the molecular mechanism(s) remains unclear, we examined the relationship between the PDK/Akt/endothelial nitric oxide synthase (NOS) pathway and endothelial function in aortas from diabetic rats that were either insulin deficient or hyperinsulinemic. |
| 1526 | 19717727 | The insulin-induced relaxation was inhibited by treatment with an Akt inhibitor in control and diabetic aortas, but not in the HI-diabetic aorta. |
| 1527 | 19717727 | In the diabetic group, various insulin-stimulated levels (nitric oxide production, phosphorylation of endothelial NOS at Ser(1177), of Akt at Thr(308), and of PDK-1 at Ser(241)) were significantly increased, whereas, in the HI-diabetic group, these levels were all decreased (vs. control aortas). |
| 1528 | 19717727 | These results suggest that the plasma insulin level has a close relation to the level of aortic PDK-1/Akt (at Thr(308))/NOS activities, and that reduced actions of the PDK-1/Akt (at Thr(308)) signal pathway may contribute to the impairments of insulin-induced endothelial functions seen in hyperinsulinemic diabetes. |
| 1529 | 19717727 | Activation of the PDK-1/Akt/eNOS pathway involved in aortic endothelial function differs between hyperinsulinemic and insulin-deficient diabetic rats. |
| 1530 | 19717727 | In diabetic states, altered plasma insulin is likely to play key roles in 3-phosphoinositide-dependent protein kinase (PDK)/Akt pathway activation, in insulin resistance and in endothelial dysfunction. |
| 1531 | 19717727 | Since the molecular mechanism(s) remains unclear, we examined the relationship between the PDK/Akt/endothelial nitric oxide synthase (NOS) pathway and endothelial function in aortas from diabetic rats that were either insulin deficient or hyperinsulinemic. |
| 1532 | 19717727 | The insulin-induced relaxation was inhibited by treatment with an Akt inhibitor in control and diabetic aortas, but not in the HI-diabetic aorta. |
| 1533 | 19717727 | In the diabetic group, various insulin-stimulated levels (nitric oxide production, phosphorylation of endothelial NOS at Ser(1177), of Akt at Thr(308), and of PDK-1 at Ser(241)) were significantly increased, whereas, in the HI-diabetic group, these levels were all decreased (vs. control aortas). |
| 1534 | 19717727 | These results suggest that the plasma insulin level has a close relation to the level of aortic PDK-1/Akt (at Thr(308))/NOS activities, and that reduced actions of the PDK-1/Akt (at Thr(308)) signal pathway may contribute to the impairments of insulin-induced endothelial functions seen in hyperinsulinemic diabetes. |
| 1535 | 19734360 | By contrast, phosphorylation of VASP only at Ser239 is seen following activation of particulate guanylate cyclase by atrial natriuretic peptide, or following activation of soluble guanylate cyclase by sodium nitroprusside, or following treatment of myocytes with cGMP analog. |
| 1536 | 19734360 | We found that basal and isoproterenol-induced VASP phosphorylation is entirely unchanged in cardiomyocytes isolated from either endothelial or neuronal nitric oxide synthase knockout mice. |
| 1537 | 19923416 | However, the exact nitric oxide synthase (NOS) isoform regulating Q(O(2)), hemodynamics, and excretory function in the diabetic kidney remains unclear. |
| 1538 | 20060403 | We propose that nitric oxide synthase (NOS) expressed within the vascular wall is a target of estrogen action. |
| 1539 | 20363891 | Sensitivity of NOS-dependent vascular relaxation pathway to mineralocorticoid receptor blockade in caveolin-1-deficient mice. |
| 1540 | 20363891 | Endothelial caveolin-1 (cav-1) is an anchoring protein in plasma membrane caveolae where it binds endothelial nitric oxide synthase (eNOS) and limits its activation, particularly in animals fed a high salt (HS) diet. |
| 1541 | 20363891 | Cav-1 also interacts with steroid receptors such as the mineralocorticoid receptor (MR). |
| 1542 | 20363891 | Thus in cav-1 deficiency states and HS diet MR blockade is associated with increased BP, enhanced vasoconstriction, and decreased NOS-mediated vascular relaxation and eNOS expression. |
| 1543 | 20363891 | Sensitivity of NOS-dependent vascular relaxation pathway to mineralocorticoid receptor blockade in caveolin-1-deficient mice. |
| 1544 | 20363891 | Endothelial caveolin-1 (cav-1) is an anchoring protein in plasma membrane caveolae where it binds endothelial nitric oxide synthase (eNOS) and limits its activation, particularly in animals fed a high salt (HS) diet. |
| 1545 | 20363891 | Cav-1 also interacts with steroid receptors such as the mineralocorticoid receptor (MR). |
| 1546 | 20363891 | Thus in cav-1 deficiency states and HS diet MR blockade is associated with increased BP, enhanced vasoconstriction, and decreased NOS-mediated vascular relaxation and eNOS expression. |
| 1547 | 20625972 | The HUVECs were exposed to various glucose concentrations (5, 15, 30, and 60 mmol/L of D-glucose supplemented), and several oxidative stress factors, such as NO, NOS, and ROS, and inflammatory signaling markers, such as TNF-α, TNFR, RIP, TRADD, TRAF-2 and NF-κB, were analyzed at various times (24, 48, 72, and 96 h). |
| 1548 | 20721817 | This conference report highlights selected presentations on NR2B subtype-selective NMDA receptor antagonists from Merck; selective neuronal nitric oxide synthase inhibitors from Northwestern University; novel GPR119 agonists, suchas GSK-1292263A (GlaxoSmithKline plc), PSN-821 ((OSI) Prosidion) and MBX-2982 (Metabolex Inc); a small-molecule Bcl inhibitor,navitoclax (Abbott Laboratories); and p53-targeting agents from sanofi-aventis and Ascenta Therapeutics Inc, including AT-219. |
| 1549 | 20806411 | Both Epo and Epo receptor (EpoR) are expressed in the brain and are up-regulated by hypoxia. |
| 1550 | 20806411 | Hypoxia increased NO production as well as EpoR expression, and inhibition of NOS activity reduced the proportion of EpoR-expressing neurons induced at low pO(2). |
| 1551 | 20806411 | Preincubation of neurons with NO results in induction of EpoR, which gives rise to protection against hypoxia even in the absence of exogenous Epo, although at high concentration NO is toxic. |
| 1552 | 20806411 | These data provide evidence of a role for NO in Epo activity in brain and suggest links between NO production, EpoR expression, and Epo signaling in neuroprotection. |
| 1553 | 20811799 | IFNG-inducible KYN/pteridines inflammation cascade is characterized by up-regulation of nitric oxide synthase (NOS) activity (induced by KYN) and decreased formation of NOS cofactor, BH4, that results in uncoupling of NOS that shifting arginine from NO to superoxide anion production. |
| 1554 | 20811799 | IFNG-induced up-regulation of indoleamine 2,3-dioxygenase (IDO), rate-limiting enzyme of TRY-KYN pathway, decreases TRY conversion into serotonin (substrate of antidepressant effect) and increases production of KYN associated with diabetes [xanthurenic acid (XA)], anxiety (KYN), psychoses and cognitive impairment (kynurenic acid). |
| 1555 | 20811799 | In addition to literature data on KYN/TRY ratio (IDO activity index), we observe neopterin levels (index of activity of rate-limiting enzyme of guanine-BH4 pathway) to be higher in carriers of high (T) than of low (A) producers alleles; and to correlate with AAMPD markers (e.g., insulin resistance, body mass index, mortality risk), and with IFN-alpha-induced depression in hepatitis C patients. |
| 1556 | 20817212 | Glucokinase regulates insulin secretion via phosphorylation of glucose. |
| 1557 | 20817212 | The present study focused on a system for the self-protection of pancreatic cell by expressing heat shock factor (HSF) and heat shock protein (HSP) to improve insulin secretion without inducing hypoglycemia. |
| 1558 | 20817212 | CA-hHSF1 expression increased insulin secretion 1.27-fold compared with the overexpression of wild-type hHSF1 in MIN6 cells via induction of HSP90 expression and subsequent activation of glucokinase. |
| 1559 | 20817212 | This mechanism is associated with activation of both glucokinase and neuronal nitric oxide synthase. |
| 1560 | 20817701 | Intracoronary infusions of acetylcholine (ACh) and the nitric oxide synthase (NOS) inhibitor N(G)-monomethyl-l-arginine (l-NMMA) are routinely used to assess endothelial function in the human coronary circulation. |
| 1561 | 20956460 | Additionally, Chinese propolis induced an increase in the serum superoxide dismutase (SOD) level significantly while Brazilian propolis raised serum SOD and reduced level of malonaldehyde (MDA) and nitric synthetase (NOS). |
| 1562 | 21094691 | We studied nitric oxide synthase (NOS) expression in kidney of obese Zucker fa/fa rats, a model of Type 2 obesity-related DN. |
| 1563 | 21094691 | Levels of eNOS and nNOS are higher in males than females at 6 weeks on the REG diet and 13 weeks on either diet; the relationship is reversed in females at 6 weeks on the AO diet. |
| 1564 | 21094691 | Levels of eNOS and nNOS are lower on the AO diet compared to REG, in males at 6 and 13 weeks and females at 13 weeks; the reverse is seen in 6 week females and 20 week males. |
| 1565 | 21094691 | We studied nitric oxide synthase (NOS) expression in kidney of obese Zucker fa/fa rats, a model of Type 2 obesity-related DN. |
| 1566 | 21094691 | Levels of eNOS and nNOS are higher in males than females at 6 weeks on the REG diet and 13 weeks on either diet; the relationship is reversed in females at 6 weeks on the AO diet. |
| 1567 | 21094691 | Levels of eNOS and nNOS are lower on the AO diet compared to REG, in males at 6 and 13 weeks and females at 13 weeks; the reverse is seen in 6 week females and 20 week males. |
| 1568 | 21094691 | We studied nitric oxide synthase (NOS) expression in kidney of obese Zucker fa/fa rats, a model of Type 2 obesity-related DN. |
| 1569 | 21094691 | Levels of eNOS and nNOS are higher in males than females at 6 weeks on the REG diet and 13 weeks on either diet; the relationship is reversed in females at 6 weeks on the AO diet. |
| 1570 | 21094691 | Levels of eNOS and nNOS are lower on the AO diet compared to REG, in males at 6 and 13 weeks and females at 13 weeks; the reverse is seen in 6 week females and 20 week males. |
| 1571 | 21169403 | Our goal was to examine whether exercise training (ExT) could normalize impaired nitric oxide synthase (NOS)-dependent dilation of cerebral (pial) arterioles during type 1 diabetes (T1D). |
| 1572 | 21169403 | We measured the in vivo diameter of pial arterioles in sedentary and exercised nondiabetic and diabetic rats in response to an endothelial NOS (eNOS)-dependent (ADP), an neuronal NOS (nNOS)-dependent [N-methyl-D-aspartate (NMDA)], and a NOS-independent (nitroglycerin) agonist. |
| 1573 | 21169403 | Furthermore, we used Western blot analysis to determine eNOS and nNOS protein levels in cerebral vessels/brain tissue in sedentary and exercised nondiabetic and diabetic rats. |
| 1574 | 21169403 | Finally, we found that eNOS protein was increased in diabetic rats and further increased by ExT and that nNOS protein was not influenced by T1D but was increased by ExT. |
| 1575 | 21169403 | We conclude that ExT can alleviate impaired eNOS- and nNOS-dependent responses of pial arterioles during T1D. |
| 1576 | 21169403 | Our goal was to examine whether exercise training (ExT) could normalize impaired nitric oxide synthase (NOS)-dependent dilation of cerebral (pial) arterioles during type 1 diabetes (T1D). |
| 1577 | 21169403 | We measured the in vivo diameter of pial arterioles in sedentary and exercised nondiabetic and diabetic rats in response to an endothelial NOS (eNOS)-dependent (ADP), an neuronal NOS (nNOS)-dependent [N-methyl-D-aspartate (NMDA)], and a NOS-independent (nitroglycerin) agonist. |
| 1578 | 21169403 | Furthermore, we used Western blot analysis to determine eNOS and nNOS protein levels in cerebral vessels/brain tissue in sedentary and exercised nondiabetic and diabetic rats. |
| 1579 | 21169403 | Finally, we found that eNOS protein was increased in diabetic rats and further increased by ExT and that nNOS protein was not influenced by T1D but was increased by ExT. |
| 1580 | 21169403 | We conclude that ExT can alleviate impaired eNOS- and nNOS-dependent responses of pial arterioles during T1D. |
| 1581 | 21169403 | Our goal was to examine whether exercise training (ExT) could normalize impaired nitric oxide synthase (NOS)-dependent dilation of cerebral (pial) arterioles during type 1 diabetes (T1D). |
| 1582 | 21169403 | We measured the in vivo diameter of pial arterioles in sedentary and exercised nondiabetic and diabetic rats in response to an endothelial NOS (eNOS)-dependent (ADP), an neuronal NOS (nNOS)-dependent [N-methyl-D-aspartate (NMDA)], and a NOS-independent (nitroglycerin) agonist. |
| 1583 | 21169403 | Furthermore, we used Western blot analysis to determine eNOS and nNOS protein levels in cerebral vessels/brain tissue in sedentary and exercised nondiabetic and diabetic rats. |
| 1584 | 21169403 | Finally, we found that eNOS protein was increased in diabetic rats and further increased by ExT and that nNOS protein was not influenced by T1D but was increased by ExT. |
| 1585 | 21169403 | We conclude that ExT can alleviate impaired eNOS- and nNOS-dependent responses of pial arterioles during T1D. |
| 1586 | 21169403 | Our goal was to examine whether exercise training (ExT) could normalize impaired nitric oxide synthase (NOS)-dependent dilation of cerebral (pial) arterioles during type 1 diabetes (T1D). |
| 1587 | 21169403 | We measured the in vivo diameter of pial arterioles in sedentary and exercised nondiabetic and diabetic rats in response to an endothelial NOS (eNOS)-dependent (ADP), an neuronal NOS (nNOS)-dependent [N-methyl-D-aspartate (NMDA)], and a NOS-independent (nitroglycerin) agonist. |
| 1588 | 21169403 | Furthermore, we used Western blot analysis to determine eNOS and nNOS protein levels in cerebral vessels/brain tissue in sedentary and exercised nondiabetic and diabetic rats. |
| 1589 | 21169403 | Finally, we found that eNOS protein was increased in diabetic rats and further increased by ExT and that nNOS protein was not influenced by T1D but was increased by ExT. |
| 1590 | 21169403 | We conclude that ExT can alleviate impaired eNOS- and nNOS-dependent responses of pial arterioles during T1D. |
| 1591 | 21169403 | Our goal was to examine whether exercise training (ExT) could normalize impaired nitric oxide synthase (NOS)-dependent dilation of cerebral (pial) arterioles during type 1 diabetes (T1D). |
| 1592 | 21169403 | We measured the in vivo diameter of pial arterioles in sedentary and exercised nondiabetic and diabetic rats in response to an endothelial NOS (eNOS)-dependent (ADP), an neuronal NOS (nNOS)-dependent [N-methyl-D-aspartate (NMDA)], and a NOS-independent (nitroglycerin) agonist. |
| 1593 | 21169403 | Furthermore, we used Western blot analysis to determine eNOS and nNOS protein levels in cerebral vessels/brain tissue in sedentary and exercised nondiabetic and diabetic rats. |
| 1594 | 21169403 | Finally, we found that eNOS protein was increased in diabetic rats and further increased by ExT and that nNOS protein was not influenced by T1D but was increased by ExT. |
| 1595 | 21169403 | We conclude that ExT can alleviate impaired eNOS- and nNOS-dependent responses of pial arterioles during T1D. |
| 1596 | 21189167 | Effect of natural polyphenols, pycnogenol® on superoxide dismutase and nitric oxide synthase in diabetic rats. |
| 1597 | 21189167 | The work is focused on clarifying the impact of diabetes and natural plant polyphenols contained in Pycnogenol® (PYC) on the activity and synthesis of Cu/Zn-SOD and synthesis of nNOS and eNOS in the cerebellum and cerebral cortex in rats with induced diabetes. |
| 1598 | 21198553 | Similar to all NOS isoforms, functional eNOS transfers electrons from nicotinamide adenine dinucleotide phosphate (NADPH), via the flavins flavin adenine dinucleotide and flavin mononucleotide in the carboxy-terminal reductase domain, to the heme in the amino-terminal oxygenase domain. |
| 1599 | 21198553 | NADPH-oxidase-derived superoxide avidly reacts with eNOS-derived NO to form peroxynitrite (ONOO(-)). |
| 1600 | 21198553 | These include the protein kinase C inhibitor midostaurin, the pentacyclic triterpenoids ursolic acid and betulinic acid, the eNOS enhancing compounds AVE9488 and AVE3085, and the polyphenolic phytoalexin trans-resveratrol. |
| 1601 | 21234858 | Serine-1177-specific phosphorylation of NOS type 3 (NOS-3) and phosphorylation of protein kinase Akt were determined in platelets by Western blotting. |
| 1602 | 21234858 | Western blotting studies revealed that AGEs decreased NOS-3 phosphorylation on serine-1177, increased NOS-3 O-glycosylation, and decreased serine phosphorylation of protein kinase Akt; all of these changes were abrogated by pyridoxine. |
| 1603 | 21234858 | We conclude that pyridoxine is effective in ameliorating the dysfunction of platelet NO signaling in response to AGEs, through improving PI3K activity, and hence downstream Akt phosphorylation and in turn serine-1177 phosphorylation of NOS-3. |
| 1604 | 21235861 | Endothelium-derived nitric oxide (NO) is a key determinant of blood pressure homeostasis and platelet aggregation and is synthesized by the endothelial isoform of nitric oxide synthase (eNOS). |
| 1605 | 21235861 | This review summarizes recent advances in understanding the molecular regulation of eNOS and the other NOS isoforms and identifies important parallels between eNOS and other cell-signaling molecules. © 1997, Elsevier Science Inc. |
| 1606 | 21236251 | We prepared AGEs, established the high glucose-AGEs injured microEC models by MTT assay, which was further supported by significantly decreased nitric oxide (NO) release, NO synthase (NOS) and thrombomodulin production with ELISA, western blot and RT-PCR analysis. |
| 1607 | 21236251 | Berberine treatments showed significant improvements as indicated by significantly increased NO release, NOS and thrombomodulin production. |
| 1608 | 21236251 | We prepared AGEs, established the high glucose-AGEs injured microEC models by MTT assay, which was further supported by significantly decreased nitric oxide (NO) release, NO synthase (NOS) and thrombomodulin production with ELISA, western blot and RT-PCR analysis. |
| 1609 | 21236251 | Berberine treatments showed significant improvements as indicated by significantly increased NO release, NOS and thrombomodulin production. |
| 1610 | 21286662 | Our results revealed that the mRNA expressions of inducible nitric oxide synthase (iNOS) and neuronal nitric oxide synthase (nNOS) were each reduced by ~50% in Avpf-treated mice vs. the controls, whereas, the mRNA expression levels of endothelial nitric oxide synthase remained unchanged. |
| 1611 | 21286662 | These findings collectively suggest that Avpf significantly protects the gastric mucosa against ethanol-induced gastric damage, at least in part, by decreasing mRNA expression levels of not only iNOS and nNOS, but also MMP-9. |
| 1612 | 21286662 | Our results revealed that the mRNA expressions of inducible nitric oxide synthase (iNOS) and neuronal nitric oxide synthase (nNOS) were each reduced by ~50% in Avpf-treated mice vs. the controls, whereas, the mRNA expression levels of endothelial nitric oxide synthase remained unchanged. |
| 1613 | 21286662 | These findings collectively suggest that Avpf significantly protects the gastric mucosa against ethanol-induced gastric damage, at least in part, by decreasing mRNA expression levels of not only iNOS and nNOS, but also MMP-9. |
| 1614 | 21419857 | NO is synthesized by nitric oxide synthase (NOS) using l-arginine as substrate. |
| 1615 | 21554376 | Uncoupling of nitric oxide synthase (NOS) has been implicated in the pathogenesis of left ventricular (LV) dysfunction in diabetes mellitus. |
| 1616 | 21554376 | Diabetes was induced in wild-type (WT), endothelial (e) NOS knockout (eNOS(-/-)), inducible (i) NOS knockout (iNOS(-/-)) and neuronal (n) NOS knockout (nNOS(-/-)) mice by streptozotocin (STZ) treatment. 3. |
| 1617 | 21554376 | In the diabetic heart, iNOS, but not eNOS or nNOS, expression was increased. |
| 1618 | 21554376 | These results suggest that sepiapterin inhibits uncoupling of NOS and improves LV function presumably by increasing iNOS-derived nitric oxide in the diabetic heart. |
| 1619 | 21554376 | Uncoupling of nitric oxide synthase (NOS) has been implicated in the pathogenesis of left ventricular (LV) dysfunction in diabetes mellitus. |
| 1620 | 21554376 | Diabetes was induced in wild-type (WT), endothelial (e) NOS knockout (eNOS(-/-)), inducible (i) NOS knockout (iNOS(-/-)) and neuronal (n) NOS knockout (nNOS(-/-)) mice by streptozotocin (STZ) treatment. 3. |
| 1621 | 21554376 | In the diabetic heart, iNOS, but not eNOS or nNOS, expression was increased. |
| 1622 | 21554376 | These results suggest that sepiapterin inhibits uncoupling of NOS and improves LV function presumably by increasing iNOS-derived nitric oxide in the diabetic heart. |
| 1623 | 21554376 | Uncoupling of nitric oxide synthase (NOS) has been implicated in the pathogenesis of left ventricular (LV) dysfunction in diabetes mellitus. |
| 1624 | 21554376 | Diabetes was induced in wild-type (WT), endothelial (e) NOS knockout (eNOS(-/-)), inducible (i) NOS knockout (iNOS(-/-)) and neuronal (n) NOS knockout (nNOS(-/-)) mice by streptozotocin (STZ) treatment. 3. |
| 1625 | 21554376 | In the diabetic heart, iNOS, but not eNOS or nNOS, expression was increased. |
| 1626 | 21554376 | These results suggest that sepiapterin inhibits uncoupling of NOS and improves LV function presumably by increasing iNOS-derived nitric oxide in the diabetic heart. |
| 1627 | 21554376 | Uncoupling of nitric oxide synthase (NOS) has been implicated in the pathogenesis of left ventricular (LV) dysfunction in diabetes mellitus. |
| 1628 | 21554376 | Diabetes was induced in wild-type (WT), endothelial (e) NOS knockout (eNOS(-/-)), inducible (i) NOS knockout (iNOS(-/-)) and neuronal (n) NOS knockout (nNOS(-/-)) mice by streptozotocin (STZ) treatment. 3. |
| 1629 | 21554376 | In the diabetic heart, iNOS, but not eNOS or nNOS, expression was increased. |
| 1630 | 21554376 | These results suggest that sepiapterin inhibits uncoupling of NOS and improves LV function presumably by increasing iNOS-derived nitric oxide in the diabetic heart. |
| 1631 | 21620828 | We analysed the vasoconstrictor response to electrical field stimulation (EFS) and the effects of the α antagonist phentolamine, the calcitonin gene related peptide (CGRP) receptor antagonist CGRP (8-37) and the nitric oxide synthase (NOS) inhibitor L-NAME in segments from untreated and fenofibrate-treated (100 mg/kg/day) diabetic rats. |
| 1632 | 21620828 | Neuronal NOS (nNOS), phosphorylated nNOS (P-nNOS), and RAMP1 protein expression were also analysed. |
| 1633 | 21620828 | P-nNOS and RAMP1 expression were increased in segments from fenofibrate-treated rats, while nNOS expression remained unmodified. |
| 1634 | 21620828 | We analysed the vasoconstrictor response to electrical field stimulation (EFS) and the effects of the α antagonist phentolamine, the calcitonin gene related peptide (CGRP) receptor antagonist CGRP (8-37) and the nitric oxide synthase (NOS) inhibitor L-NAME in segments from untreated and fenofibrate-treated (100 mg/kg/day) diabetic rats. |
| 1635 | 21620828 | Neuronal NOS (nNOS), phosphorylated nNOS (P-nNOS), and RAMP1 protein expression were also analysed. |
| 1636 | 21620828 | P-nNOS and RAMP1 expression were increased in segments from fenofibrate-treated rats, while nNOS expression remained unmodified. |
| 1637 | 21620828 | We analysed the vasoconstrictor response to electrical field stimulation (EFS) and the effects of the α antagonist phentolamine, the calcitonin gene related peptide (CGRP) receptor antagonist CGRP (8-37) and the nitric oxide synthase (NOS) inhibitor L-NAME in segments from untreated and fenofibrate-treated (100 mg/kg/day) diabetic rats. |
| 1638 | 21620828 | Neuronal NOS (nNOS), phosphorylated nNOS (P-nNOS), and RAMP1 protein expression were also analysed. |
| 1639 | 21620828 | P-nNOS and RAMP1 expression were increased in segments from fenofibrate-treated rats, while nNOS expression remained unmodified. |
| 1640 | 21623030 | Nitric oxide (NO), synthesized from the amino acid, L-arginine by nitric oxide synthase (NOS) has received attention as a neurotransmitter in the brain. |
| 1641 | 21631419 | It is synthesized by three distinct enzymes: endothelial (eNOS), neuronal (nNOS) and inducible (iNOS) nitricoxide synthases. |
| 1642 | 21631419 | However, the activity of different NOSs isoforms as well as, the bioavailability of NO can be affected by a variety of disease conditions (in particular diabetes) and pathological situations associated with significantly elevated levels of the pro-inflammatory cytokine tumor necrosis factor-α (TNF-α). |
| 1643 | 21631419 | It is synthesized by three distinct enzymes: endothelial (eNOS), neuronal (nNOS) and inducible (iNOS) nitricoxide synthases. |
| 1644 | 21631419 | However, the activity of different NOSs isoforms as well as, the bioavailability of NO can be affected by a variety of disease conditions (in particular diabetes) and pathological situations associated with significantly elevated levels of the pro-inflammatory cytokine tumor necrosis factor-α (TNF-α). |
| 1645 | 21663490 | Nitric oxide synthase (NOS) activity was measured in kidney homogenates. |
| 1646 | 21666113 | We measured the responses of cerebral arterioles in untreated and resveratrol-treated (10 mg·kg(-1)·day(-1)) nondiabetic and diabetic rats to endothelial (eNOS) and neuronal (nNOS) nitric oxide synthase (NOS)-dependent agonists and to a NOS-independent agonist. |
| 1647 | 21666113 | Furthermore, we used Western blot analysis to determine the protein expression of eNOS, nNOS, SOD-1, and SOD-2 in cerebral arterioles and/or brain tissue from untreated and resveratrol-treated nondiabetic and diabetic rats. |
| 1648 | 21666113 | We found that T1D impaired eNOS- and nNOS-dependent reactivity of cerebral arterioles but did not alter NOS-independent vasodilation. |
| 1649 | 21666113 | While resveratrol did not alter responses in nondiabetic rats, resveratrol prevented T1D-induced impairment in eNOS- and nNOS-dependent vasodilation. |
| 1650 | 21666113 | Furthermore, eNOS and nNOS protein were increased in diabetic rats and resveratrol produced a further increased eNOS and nNOS proteins. |
| 1651 | 21666113 | SOD-1 and SOD-2 proteins were not altered by T1D, but resveratrol treatment produced a decrease in SOD-2 protein. |
| 1652 | 21666113 | We measured the responses of cerebral arterioles in untreated and resveratrol-treated (10 mg·kg(-1)·day(-1)) nondiabetic and diabetic rats to endothelial (eNOS) and neuronal (nNOS) nitric oxide synthase (NOS)-dependent agonists and to a NOS-independent agonist. |
| 1653 | 21666113 | Furthermore, we used Western blot analysis to determine the protein expression of eNOS, nNOS, SOD-1, and SOD-2 in cerebral arterioles and/or brain tissue from untreated and resveratrol-treated nondiabetic and diabetic rats. |
| 1654 | 21666113 | We found that T1D impaired eNOS- and nNOS-dependent reactivity of cerebral arterioles but did not alter NOS-independent vasodilation. |
| 1655 | 21666113 | While resveratrol did not alter responses in nondiabetic rats, resveratrol prevented T1D-induced impairment in eNOS- and nNOS-dependent vasodilation. |
| 1656 | 21666113 | Furthermore, eNOS and nNOS protein were increased in diabetic rats and resveratrol produced a further increased eNOS and nNOS proteins. |
| 1657 | 21666113 | SOD-1 and SOD-2 proteins were not altered by T1D, but resveratrol treatment produced a decrease in SOD-2 protein. |
| 1658 | 21666113 | We measured the responses of cerebral arterioles in untreated and resveratrol-treated (10 mg·kg(-1)·day(-1)) nondiabetic and diabetic rats to endothelial (eNOS) and neuronal (nNOS) nitric oxide synthase (NOS)-dependent agonists and to a NOS-independent agonist. |
| 1659 | 21666113 | Furthermore, we used Western blot analysis to determine the protein expression of eNOS, nNOS, SOD-1, and SOD-2 in cerebral arterioles and/or brain tissue from untreated and resveratrol-treated nondiabetic and diabetic rats. |
| 1660 | 21666113 | We found that T1D impaired eNOS- and nNOS-dependent reactivity of cerebral arterioles but did not alter NOS-independent vasodilation. |
| 1661 | 21666113 | While resveratrol did not alter responses in nondiabetic rats, resveratrol prevented T1D-induced impairment in eNOS- and nNOS-dependent vasodilation. |
| 1662 | 21666113 | Furthermore, eNOS and nNOS protein were increased in diabetic rats and resveratrol produced a further increased eNOS and nNOS proteins. |
| 1663 | 21666113 | SOD-1 and SOD-2 proteins were not altered by T1D, but resveratrol treatment produced a decrease in SOD-2 protein. |
| 1664 | 21666113 | We measured the responses of cerebral arterioles in untreated and resveratrol-treated (10 mg·kg(-1)·day(-1)) nondiabetic and diabetic rats to endothelial (eNOS) and neuronal (nNOS) nitric oxide synthase (NOS)-dependent agonists and to a NOS-independent agonist. |
| 1665 | 21666113 | Furthermore, we used Western blot analysis to determine the protein expression of eNOS, nNOS, SOD-1, and SOD-2 in cerebral arterioles and/or brain tissue from untreated and resveratrol-treated nondiabetic and diabetic rats. |
| 1666 | 21666113 | We found that T1D impaired eNOS- and nNOS-dependent reactivity of cerebral arterioles but did not alter NOS-independent vasodilation. |
| 1667 | 21666113 | While resveratrol did not alter responses in nondiabetic rats, resveratrol prevented T1D-induced impairment in eNOS- and nNOS-dependent vasodilation. |
| 1668 | 21666113 | Furthermore, eNOS and nNOS protein were increased in diabetic rats and resveratrol produced a further increased eNOS and nNOS proteins. |
| 1669 | 21666113 | SOD-1 and SOD-2 proteins were not altered by T1D, but resveratrol treatment produced a decrease in SOD-2 protein. |
| 1670 | 21666113 | We measured the responses of cerebral arterioles in untreated and resveratrol-treated (10 mg·kg(-1)·day(-1)) nondiabetic and diabetic rats to endothelial (eNOS) and neuronal (nNOS) nitric oxide synthase (NOS)-dependent agonists and to a NOS-independent agonist. |
| 1671 | 21666113 | Furthermore, we used Western blot analysis to determine the protein expression of eNOS, nNOS, SOD-1, and SOD-2 in cerebral arterioles and/or brain tissue from untreated and resveratrol-treated nondiabetic and diabetic rats. |
| 1672 | 21666113 | We found that T1D impaired eNOS- and nNOS-dependent reactivity of cerebral arterioles but did not alter NOS-independent vasodilation. |
| 1673 | 21666113 | While resveratrol did not alter responses in nondiabetic rats, resveratrol prevented T1D-induced impairment in eNOS- and nNOS-dependent vasodilation. |
| 1674 | 21666113 | Furthermore, eNOS and nNOS protein were increased in diabetic rats and resveratrol produced a further increased eNOS and nNOS proteins. |
| 1675 | 21666113 | SOD-1 and SOD-2 proteins were not altered by T1D, but resveratrol treatment produced a decrease in SOD-2 protein. |
| 1676 | 21729132 | Icarisid II, a PDE5 inhibitor from Epimedium wanshanense, increases cellular cGMP by enhancing NOS in diabetic ED rats corpus cavernosum tissue. |
| 1677 | 21729132 | The RCCT was treated with ICA-II, ICA and Sildenafil at different concentrations. cGMP and nitric oxide synthase (NOS) activities were checked respectively by enzyme immunoassay. |
| 1678 | 21729132 | Meanwhile, nNOS, iNOS and eNOS in RCCT were checked by western blot. |
| 1679 | 21729132 | With the treatment of 10 μm ICA-II for 24 and 48 h, nNOS expression was significantly increased in RCCT (P < 0.05), while the eNOS expression level was very low without any change. |
| 1680 | 21729132 | Except the PDE5 inhibitory effect, ICA-II increases the intracellular cGMP through the enhancement of nNOS expression and NOS activity in RCCT in vitro. |
| 1681 | 21729132 | Icarisid II, a PDE5 inhibitor from Epimedium wanshanense, increases cellular cGMP by enhancing NOS in diabetic ED rats corpus cavernosum tissue. |
| 1682 | 21729132 | The RCCT was treated with ICA-II, ICA and Sildenafil at different concentrations. cGMP and nitric oxide synthase (NOS) activities were checked respectively by enzyme immunoassay. |
| 1683 | 21729132 | Meanwhile, nNOS, iNOS and eNOS in RCCT were checked by western blot. |
| 1684 | 21729132 | With the treatment of 10 μm ICA-II for 24 and 48 h, nNOS expression was significantly increased in RCCT (P < 0.05), while the eNOS expression level was very low without any change. |
| 1685 | 21729132 | Except the PDE5 inhibitory effect, ICA-II increases the intracellular cGMP through the enhancement of nNOS expression and NOS activity in RCCT in vitro. |
| 1686 | 21729132 | Icarisid II, a PDE5 inhibitor from Epimedium wanshanense, increases cellular cGMP by enhancing NOS in diabetic ED rats corpus cavernosum tissue. |
| 1687 | 21729132 | The RCCT was treated with ICA-II, ICA and Sildenafil at different concentrations. cGMP and nitric oxide synthase (NOS) activities were checked respectively by enzyme immunoassay. |
| 1688 | 21729132 | Meanwhile, nNOS, iNOS and eNOS in RCCT were checked by western blot. |
| 1689 | 21729132 | With the treatment of 10 μm ICA-II for 24 and 48 h, nNOS expression was significantly increased in RCCT (P < 0.05), while the eNOS expression level was very low without any change. |
| 1690 | 21729132 | Except the PDE5 inhibitory effect, ICA-II increases the intracellular cGMP through the enhancement of nNOS expression and NOS activity in RCCT in vitro. |
| 1691 | 21729132 | Icarisid II, a PDE5 inhibitor from Epimedium wanshanense, increases cellular cGMP by enhancing NOS in diabetic ED rats corpus cavernosum tissue. |
| 1692 | 21729132 | The RCCT was treated with ICA-II, ICA and Sildenafil at different concentrations. cGMP and nitric oxide synthase (NOS) activities were checked respectively by enzyme immunoassay. |
| 1693 | 21729132 | Meanwhile, nNOS, iNOS and eNOS in RCCT were checked by western blot. |
| 1694 | 21729132 | With the treatment of 10 μm ICA-II for 24 and 48 h, nNOS expression was significantly increased in RCCT (P < 0.05), while the eNOS expression level was very low without any change. |
| 1695 | 21729132 | Except the PDE5 inhibitory effect, ICA-II increases the intracellular cGMP through the enhancement of nNOS expression and NOS activity in RCCT in vitro. |
| 1696 | 21729132 | Icarisid II, a PDE5 inhibitor from Epimedium wanshanense, increases cellular cGMP by enhancing NOS in diabetic ED rats corpus cavernosum tissue. |
| 1697 | 21729132 | The RCCT was treated with ICA-II, ICA and Sildenafil at different concentrations. cGMP and nitric oxide synthase (NOS) activities were checked respectively by enzyme immunoassay. |
| 1698 | 21729132 | Meanwhile, nNOS, iNOS and eNOS in RCCT were checked by western blot. |
| 1699 | 21729132 | With the treatment of 10 μm ICA-II for 24 and 48 h, nNOS expression was significantly increased in RCCT (P < 0.05), while the eNOS expression level was very low without any change. |
| 1700 | 21729132 | Except the PDE5 inhibitory effect, ICA-II increases the intracellular cGMP through the enhancement of nNOS expression and NOS activity in RCCT in vitro. |
| 1701 | 21756052 | Oxidative stress may cause a loss of tetrahydrobiopterin (BH4), a co-factor of nitric oxide synthase (NOS), decrease the bioavailability of NO and aggravate ischemia/reperfusion (I/R) injury in diabetic heart. |
| 1702 | 21792376 | Regulation of Inducible Nitric Oxide Synthase (iNOS) and its Potential Role in Insulin Resistance, Diabetes and Heart Failure. |
| 1703 | 21792376 | In mammals 3 distinct isoforms of NOS have been identified: neuronal NOS (nNOS), inducible NOS (iNOS) and endothelial NOS (eNOS). |
| 1704 | 21792376 | The important isoform in the regulation of insulin resistance (IR) is iNOS. |
| 1705 | 21873498 | To test the hypothesis that LSD1 plays a role in the regulation of blood pressure (BP) via vascular mechanisms and gene transcription, we measured BP and examined vascular function and endothelial nitric oxide (NO) synthase (eNOS) expression in thoracic aorta of male wild-type (WT) and heterozygous LSD1 knockout mice (LSD1(+/-)) fed either a liberal salt (HS; 4% NaCl) or restricted salt diet (LS; 0.08% NaCl). |
| 1706 | 21873498 | Further examination of the mechanisms of this salt-sensitive hypertension in LSD1(+/-) mice on the HS diet demonstrated that plasma renin activity and plasma levels and urinary excretion of aldosterone were less in LSD1(+/-) than WT, suggesting suppressed renin-angiotensin-aldosterone system. |
| 1707 | 21873498 | Endothelium removal or pretreatment with N(ω)-nitro-L-arginine methyl ester (blocker of NOS) or ODQ abolished Ach-induced relaxation in aorta of WT but had minimal effect in LSD1(+/-). |
| 1708 | 21873498 | RT-PCR and Western blots revealed decreased eNOS mRNA expression and eNOS and guanylate cyclase protein in the heart and aorta of LSD1(+/-) compared with WT mice on HS diet. |
| 1709 | 21873498 | The data support a role for LSD1-mediated histone demethylation in the regulation of NOS/guanylate cyclase gene expression, vascular function, and BP during the HS diet. |
| 1710 | 21873498 | To test the hypothesis that LSD1 plays a role in the regulation of blood pressure (BP) via vascular mechanisms and gene transcription, we measured BP and examined vascular function and endothelial nitric oxide (NO) synthase (eNOS) expression in thoracic aorta of male wild-type (WT) and heterozygous LSD1 knockout mice (LSD1(+/-)) fed either a liberal salt (HS; 4% NaCl) or restricted salt diet (LS; 0.08% NaCl). |
| 1711 | 21873498 | Further examination of the mechanisms of this salt-sensitive hypertension in LSD1(+/-) mice on the HS diet demonstrated that plasma renin activity and plasma levels and urinary excretion of aldosterone were less in LSD1(+/-) than WT, suggesting suppressed renin-angiotensin-aldosterone system. |
| 1712 | 21873498 | Endothelium removal or pretreatment with N(ω)-nitro-L-arginine methyl ester (blocker of NOS) or ODQ abolished Ach-induced relaxation in aorta of WT but had minimal effect in LSD1(+/-). |
| 1713 | 21873498 | RT-PCR and Western blots revealed decreased eNOS mRNA expression and eNOS and guanylate cyclase protein in the heart and aorta of LSD1(+/-) compared with WT mice on HS diet. |
| 1714 | 21873498 | The data support a role for LSD1-mediated histone demethylation in the regulation of NOS/guanylate cyclase gene expression, vascular function, and BP during the HS diet. |
| 1715 | 21964072 | Insulin treatment restored ischemia-induced release of stromal-derived growth factor 1α and vascular endothelial growth factor (VEGF), and consequently enhanced the activity of Akt and endothelial nitric oxide synthase (eNOS) as well as matrix metalloproteinase-9 in bone marrow. |
| 1716 | 21964072 | Insulin also augmented tissue-level activation of VEGF/Akt/eNOS pathway. |
| 1717 | 21964072 | However, all such effects of insulin were completely blocked by combined treatment with a NOS inhibitor. |
| 1718 | 21964072 | Our data suggested that insulin treatment improved ischemia-induced EPC mobilization and contributed to compensatory neovascularization in diabetic mice through a VEGF/eNOS-related pathway. |
| 1719 | 21972802 | SalA treatment also reduced the serum malondialdehyde, the content of aortic advanced glycation end products (AGEs), and the nitric oxide synthase (NOS) activity as well as the expression of endothelial NOS protein in the rat aorta. |
| 1720 | 21975567 | Cavernosal strips from nNOS- and endothelial nitric oxide synthase (eNOS)-knockout (KO) mice, besides nNOS inhibitor (10(-5) M), were used to evaluate the role of this enzyme in the potentiation effect evoked by PnTx2-6. |
| 1721 | 21975567 | Results showed that PnTx2-6 enhanced cavernosal relaxation in diabetic mice (65%) and eNOS KO mice, but not in nNOS KO mice. |
| 1722 | 21975567 | Cavernosal strips from nNOS- and endothelial nitric oxide synthase (eNOS)-knockout (KO) mice, besides nNOS inhibitor (10(-5) M), were used to evaluate the role of this enzyme in the potentiation effect evoked by PnTx2-6. |
| 1723 | 21975567 | Results showed that PnTx2-6 enhanced cavernosal relaxation in diabetic mice (65%) and eNOS KO mice, but not in nNOS KO mice. |
| 1724 | 22357961 | After confirming that GLP-1 potently stimulates nitric oxide (NO) synthase (NOS) phosphorylation in endothelial cells, overnight-fasted adult male rats received continuous GLP-1 infusion (30 pmol/kg/min) for 2 h plus or minus NOS inhibition. |
| 1725 | 22357961 | Additional rats received GLP-1 or saline for 30 min and muscle insulin clearance/uptake was determined. |
| 1726 | 22357961 | NOS inhibition blocked GLP-1-mediated increases in muscle MBV, glucose disposal, NO production, and muscle insulin clearance/uptake. |
| 1727 | 22357961 | Thus, GLP-1 may afford potential to improve muscle insulin action by expanding microvascular endothelial surface area. |
| 1728 | 22357961 | After confirming that GLP-1 potently stimulates nitric oxide (NO) synthase (NOS) phosphorylation in endothelial cells, overnight-fasted adult male rats received continuous GLP-1 infusion (30 pmol/kg/min) for 2 h plus or minus NOS inhibition. |
| 1729 | 22357961 | Additional rats received GLP-1 or saline for 30 min and muscle insulin clearance/uptake was determined. |
| 1730 | 22357961 | NOS inhibition blocked GLP-1-mediated increases in muscle MBV, glucose disposal, NO production, and muscle insulin clearance/uptake. |
| 1731 | 22357961 | Thus, GLP-1 may afford potential to improve muscle insulin action by expanding microvascular endothelial surface area. |
| 1732 | 22361333 | Nitric oxide synthase enzyme (NOS) possesses the unique ability to be "uncoupled" to produce superoxide anion (O(2)(-)) instead of nitric oxide (NO). |
| 1733 | 22403279 | Penises were harvested with subsequent histological examination (picrosirius red stain, Hart elastin stain, and immunohistochemical stain) and Western blots to explore the expression of the nitric oxide-cyclic guanosine monophosphate (NO-cGMP) and transforming growth factor β1 (TGFβ1)/Smad2 signaling pathways. |
| 1734 | 22403279 | The ratio of collagen I to III was significantly lower in the corpora of diabetic rats; furthermore, cavernous elastic fibers were fragmented in the diabetic animals. |
| 1735 | 22403279 | Neuronal nitric oxide synthase (nNOS), endothelial nitric oxide synthase, and vascular endothelial growth factor were expressed at lower levels in the diabetic group; ICA II-treated diabetic rats had higher expression in the penis relative to placebo-treated diabetic animals. |
| 1736 | 22403279 | Both the TGFβ1/Smad2/connective tissue growth factor (CTGF) signaling pathway and apoptosis were down-regulated in the penis from ICA II-treated rats. |
| 1737 | 22403279 | ICA II could alter corpus cavernosum fibrous-muscular pathological structure in diabetic rats, which could be regulated by the TGFβ1/Smad2/CTGF and NO-cGMP signaling pathways. |
| 1738 | 22498644 | Although we have found the participation of nitric oxide synthase (NOS) activation as a mechanism of the decrease in intestinal P-gp expression under diabetic conditions, more detailed mechanisms other than NOS remain unknown. |
| 1739 | 22498644 | Here, we studied the involvement of the ubiquitin-proteasome system in the mechanism of the decrease in intestinal P-gp expression under diabetic conditions. |
| 1740 | 22498644 | Our results reveal the participation of the acceleration of the ubiquitin-preotasome system by NO in the decrease of intestinal P-gp expression levels under diabetic conditions. |
| 1741 | 22554865 | Retinal function (electroretinogram, ERG) and morphology (optical microscopy), retinal nitric oxide synthase (NOS) activity (using (3)H-arginine), lipid peroxidation (thiobarbituric acid reactive substances, TBARS), and TNFα levels (ELISA) were evaluated. |
| 1742 | 22554865 | At 12 weeks of treatment, a significant decrease in the ERG a- and b- wave and oscillatory potential amplitudes, and a significant increase in retinal NOS activity, TBARS, TNFα, glial fibrillary acidic protein in Müller cells, and vascular endothelial growth factor levels were observed. |
| 1743 | 22554865 | Retinal function (electroretinogram, ERG) and morphology (optical microscopy), retinal nitric oxide synthase (NOS) activity (using (3)H-arginine), lipid peroxidation (thiobarbituric acid reactive substances, TBARS), and TNFα levels (ELISA) were evaluated. |
| 1744 | 22554865 | At 12 weeks of treatment, a significant decrease in the ERG a- and b- wave and oscillatory potential amplitudes, and a significant increase in retinal NOS activity, TBARS, TNFα, glial fibrillary acidic protein in Müller cells, and vascular endothelial growth factor levels were observed. |
| 1745 | 22573263 | In addition, peak phosphorylation of the NR1 subunit of N-methyl-D-aspartate receptor (NMDAR), along with upregulation of neuronal and inducible nitric oxide synthase (nNOS and iNOS) expression were detected in diabetic mice. |
| 1746 | 22573263 | Expression of nNOS and iNOS was detected in both interneurons and astrocytes in lamina I-III of the LSCDH. |
| 1747 | 22573263 | Treatment with MK801, an NMDAR inhibitor, inhibited mechanical allodynia, ERK1/2 phosphorylation, and nNOS and iNOS upregulation in diabetic mice. |
| 1748 | 22573263 | In addition, peak phosphorylation of the NR1 subunit of N-methyl-D-aspartate receptor (NMDAR), along with upregulation of neuronal and inducible nitric oxide synthase (nNOS and iNOS) expression were detected in diabetic mice. |
| 1749 | 22573263 | Expression of nNOS and iNOS was detected in both interneurons and astrocytes in lamina I-III of the LSCDH. |
| 1750 | 22573263 | Treatment with MK801, an NMDAR inhibitor, inhibited mechanical allodynia, ERK1/2 phosphorylation, and nNOS and iNOS upregulation in diabetic mice. |
| 1751 | 22573263 | In addition, peak phosphorylation of the NR1 subunit of N-methyl-D-aspartate receptor (NMDAR), along with upregulation of neuronal and inducible nitric oxide synthase (nNOS and iNOS) expression were detected in diabetic mice. |
| 1752 | 22573263 | Expression of nNOS and iNOS was detected in both interneurons and astrocytes in lamina I-III of the LSCDH. |
| 1753 | 22573263 | Treatment with MK801, an NMDAR inhibitor, inhibited mechanical allodynia, ERK1/2 phosphorylation, and nNOS and iNOS upregulation in diabetic mice. |
| 1754 | 22610171 | Capsaicin (1-100 μg·kg(-1)·min(-1)) dose dependently increased coronary blood flow in control mice, which was inhibited by the TRPV1 antagonist capsazepine or the nitric oxide synthase (NOS) inhibitor N-nitro-l-arginine methyl ester (L-NAME). |
| 1755 | 22679517 | The GPR30 agonist G1 induced a dose-dependent vasodilation in the thoracic aorta of the diabetic OVX rats, which was partially attenuated by the nitric oxide synthase (NOS) inhibitor, nitro-L-arginine methylester (L-NAME) and the GPR30-selective antagonist G15. |
| 1756 | 22679517 | These findings provide preliminary evidence that GPR30 activation leads to eNOS activation, as well as vasodilation, to a certain degree and has beneficial effects on vascular function in diabetic OVX rats. |
| 1757 | 22728670 | AGE concentrations, nitric oxide synthase (NOS) activity and cGMP concentration were assessed by enzyme immunoassay. |
| 1758 | 22728670 | Our results have shown that Icarisid II increased ICP/MAP values, the smooth muscle cell (SMC) growth curve, S phase and SMC/collagen fibril (SMC/CF) proportions and decreased Beclin 1 (P<0.05). |
| 1759 | 22858624 | Thus our goal was to examine whether modest ExT could influence transient focal ischemia-induced brain injury along with nitric oxide synthase (NOS)-dependent dilation of cerebral (pial) arterioles during T1D. |
| 1760 | 22858624 | In a second series of studies, a craniotomy was performed over the parietal cortex, and we measured responses of pial arterioles to an endothelial NOS (eNOS)-dependent, a neuronal NOS (nNOS)-dependent, and a NOS-independent agonist in all groups of rats. |
| 1761 | 22858624 | In addition, ExT diabetic rats had impaired eNOS- and nNOS-dependent, but not NOS-independent, vasodilation that was restored by ExT. |
| 1762 | 22858624 | Thus ExT of T1D rats lessened ischemic brain injury following middle cerebral artery occlusion and restored impaired eNOS- and nNOS-dependent vascular function. |
| 1763 | 22858624 | Thus our goal was to examine whether modest ExT could influence transient focal ischemia-induced brain injury along with nitric oxide synthase (NOS)-dependent dilation of cerebral (pial) arterioles during T1D. |
| 1764 | 22858624 | In a second series of studies, a craniotomy was performed over the parietal cortex, and we measured responses of pial arterioles to an endothelial NOS (eNOS)-dependent, a neuronal NOS (nNOS)-dependent, and a NOS-independent agonist in all groups of rats. |
| 1765 | 22858624 | In addition, ExT diabetic rats had impaired eNOS- and nNOS-dependent, but not NOS-independent, vasodilation that was restored by ExT. |
| 1766 | 22858624 | Thus ExT of T1D rats lessened ischemic brain injury following middle cerebral artery occlusion and restored impaired eNOS- and nNOS-dependent vascular function. |
| 1767 | 22858624 | Thus our goal was to examine whether modest ExT could influence transient focal ischemia-induced brain injury along with nitric oxide synthase (NOS)-dependent dilation of cerebral (pial) arterioles during T1D. |
| 1768 | 22858624 | In a second series of studies, a craniotomy was performed over the parietal cortex, and we measured responses of pial arterioles to an endothelial NOS (eNOS)-dependent, a neuronal NOS (nNOS)-dependent, and a NOS-independent agonist in all groups of rats. |
| 1769 | 22858624 | In addition, ExT diabetic rats had impaired eNOS- and nNOS-dependent, but not NOS-independent, vasodilation that was restored by ExT. |
| 1770 | 22858624 | Thus ExT of T1D rats lessened ischemic brain injury following middle cerebral artery occlusion and restored impaired eNOS- and nNOS-dependent vascular function. |
| 1771 | 22858624 | Thus our goal was to examine whether modest ExT could influence transient focal ischemia-induced brain injury along with nitric oxide synthase (NOS)-dependent dilation of cerebral (pial) arterioles during T1D. |
| 1772 | 22858624 | In a second series of studies, a craniotomy was performed over the parietal cortex, and we measured responses of pial arterioles to an endothelial NOS (eNOS)-dependent, a neuronal NOS (nNOS)-dependent, and a NOS-independent agonist in all groups of rats. |
| 1773 | 22858624 | In addition, ExT diabetic rats had impaired eNOS- and nNOS-dependent, but not NOS-independent, vasodilation that was restored by ExT. |
| 1774 | 22858624 | Thus ExT of T1D rats lessened ischemic brain injury following middle cerebral artery occlusion and restored impaired eNOS- and nNOS-dependent vascular function. |
| 1775 | 22915345 | Retinopathy, a common complication of diabetes, is characterized by an unbalanced production of nitric oxide (NO), a process regulated by nitric oxide synthase (NOS). |
| 1776 | 22915345 | We hypothesized that retinopathy might stem from changes in the insulin receptor substrate (IRS)/PI3K/AKT pathway and/or expression of NOS isoforms. |
| 1777 | 22915345 | Immunoblotting analysis revealed that the retinal tissue of HFD rats had lower levels of AKT(1) , eNOS and nNOS protein than those of samples taken from control animals. |
| 1778 | 22915345 | Retinopathy, a common complication of diabetes, is characterized by an unbalanced production of nitric oxide (NO), a process regulated by nitric oxide synthase (NOS). |
| 1779 | 22915345 | We hypothesized that retinopathy might stem from changes in the insulin receptor substrate (IRS)/PI3K/AKT pathway and/or expression of NOS isoforms. |
| 1780 | 22915345 | Immunoblotting analysis revealed that the retinal tissue of HFD rats had lower levels of AKT(1) , eNOS and nNOS protein than those of samples taken from control animals. |
| 1781 | 22915345 | Retinopathy, a common complication of diabetes, is characterized by an unbalanced production of nitric oxide (NO), a process regulated by nitric oxide synthase (NOS). |
| 1782 | 22915345 | We hypothesized that retinopathy might stem from changes in the insulin receptor substrate (IRS)/PI3K/AKT pathway and/or expression of NOS isoforms. |
| 1783 | 22915345 | Immunoblotting analysis revealed that the retinal tissue of HFD rats had lower levels of AKT(1) , eNOS and nNOS protein than those of samples taken from control animals. |
| 1784 | 22921991 | Expression of different isoforms of nitric oxide synthase in insulin-secreting INS1E cells and rat islets was analyzed by quantitative real-time PCR and Western blotting. |
| 1785 | 22921991 | The expression of nNOS in insulin-secreting INS1E cells was similar to that found in rat brain, while two other isoforms, namely the endothelial eNOS and inducible iNOS were not expressed in untreated cells. |
| 1786 | 22921991 | IL-1β alone or in combination with TNF-α and/or IFNγ induced iNOS but not eNOS expression. |
| 1787 | 22921991 | In contrast, nNOS expression was strongly decreased by the mixture of the three proinflammatory cytokines (IL-1β, TNF-α and IFNγ) both on the gene and protein level in INS1E cells and rat islet cells. |
| 1788 | 22921991 | The effects of cytokines on glucose-induced insulin-secretion followed the pattern of nNOS expression reduction and, on the other hand, of the iNOS induction. |
| 1789 | 22921991 | This nNOS suppression can compensate for NO generation by low concentrations of IL-1β through iNOS induction. |
| 1790 | 22921991 | Expression of different isoforms of nitric oxide synthase in insulin-secreting INS1E cells and rat islets was analyzed by quantitative real-time PCR and Western blotting. |
| 1791 | 22921991 | The expression of nNOS in insulin-secreting INS1E cells was similar to that found in rat brain, while two other isoforms, namely the endothelial eNOS and inducible iNOS were not expressed in untreated cells. |
| 1792 | 22921991 | IL-1β alone or in combination with TNF-α and/or IFNγ induced iNOS but not eNOS expression. |
| 1793 | 22921991 | In contrast, nNOS expression was strongly decreased by the mixture of the three proinflammatory cytokines (IL-1β, TNF-α and IFNγ) both on the gene and protein level in INS1E cells and rat islet cells. |
| 1794 | 22921991 | The effects of cytokines on glucose-induced insulin-secretion followed the pattern of nNOS expression reduction and, on the other hand, of the iNOS induction. |
| 1795 | 22921991 | This nNOS suppression can compensate for NO generation by low concentrations of IL-1β through iNOS induction. |
| 1796 | 22921991 | Expression of different isoforms of nitric oxide synthase in insulin-secreting INS1E cells and rat islets was analyzed by quantitative real-time PCR and Western blotting. |
| 1797 | 22921991 | The expression of nNOS in insulin-secreting INS1E cells was similar to that found in rat brain, while two other isoforms, namely the endothelial eNOS and inducible iNOS were not expressed in untreated cells. |
| 1798 | 22921991 | IL-1β alone or in combination with TNF-α and/or IFNγ induced iNOS but not eNOS expression. |
| 1799 | 22921991 | In contrast, nNOS expression was strongly decreased by the mixture of the three proinflammatory cytokines (IL-1β, TNF-α and IFNγ) both on the gene and protein level in INS1E cells and rat islet cells. |
| 1800 | 22921991 | The effects of cytokines on glucose-induced insulin-secretion followed the pattern of nNOS expression reduction and, on the other hand, of the iNOS induction. |
| 1801 | 22921991 | This nNOS suppression can compensate for NO generation by low concentrations of IL-1β through iNOS induction. |
| 1802 | 22921991 | Expression of different isoforms of nitric oxide synthase in insulin-secreting INS1E cells and rat islets was analyzed by quantitative real-time PCR and Western blotting. |
| 1803 | 22921991 | The expression of nNOS in insulin-secreting INS1E cells was similar to that found in rat brain, while two other isoforms, namely the endothelial eNOS and inducible iNOS were not expressed in untreated cells. |
| 1804 | 22921991 | IL-1β alone or in combination with TNF-α and/or IFNγ induced iNOS but not eNOS expression. |
| 1805 | 22921991 | In contrast, nNOS expression was strongly decreased by the mixture of the three proinflammatory cytokines (IL-1β, TNF-α and IFNγ) both on the gene and protein level in INS1E cells and rat islet cells. |
| 1806 | 22921991 | The effects of cytokines on glucose-induced insulin-secretion followed the pattern of nNOS expression reduction and, on the other hand, of the iNOS induction. |
| 1807 | 22921991 | This nNOS suppression can compensate for NO generation by low concentrations of IL-1β through iNOS induction. |
| 1808 | 23018631 | These genes belong to three major classes: genes involved in drug metabolism and transporters that influence pharmacokinetics (including the cytochrome P450 [CYP] superfamily, the organic anion transporting polypeptide [OATP] family, and the polyspecific organic cation transporter [OCT] family); genes encoding drug targets and receptors (including peroxisome proliferator-activated receptor gamma [PPARG], the adenosine triphosphate [ATP]-sensitive potassium channel [K(ATP)], and incretin receptors); and genes involved in the causal pathway of T2DM that are able to modify the effects of drugs (including adipokines, transcription factor 7-like 2 (T cell specific, HMG-box) [TCF7L2], insulin receptor substrate 1 [IRS1], nitric oxide synthase 1 (neuronal) adaptor protein [NOS1AP], and solute carrier family 30 (zinc transporter), member 8 [SLC30A8]). |
| 1809 | 23018631 | In addition to these three major classes, we also review the available evidence on novel genes (CDK5 regulatory subunit associated protein 1-like 1 [CDKAL1], insulin-like growth factor 2 mRNA binding protein 2 [IGF2BP2], potassium voltage-gated channel, KQT-like subfamily, member 1 [KCNQ1], paired box 4 [PAX4] and neuronal differentiation 1 [NEUROD1] transcription factors, ataxia telangiectasia mutated [ATM], and serine racemase [SRR]) that have recently been proposed as possible modulators of therapeutic response in subjects with T2DM. |
| 1810 | 23202294 | Activation of calcium signaling through Trpv1 by nNOS and peroxynitrite as a key trigger of skeletal muscle hypertrophy. |
| 1811 | 23202294 | Here we show that neuronal nitric oxide synthase (nNOS) regulates load-induced hypertrophy by activating transient receptor potential cation channel, subfamily V, member 1 (TRPV1). |
| 1812 | 23202294 | Activation of calcium signaling through Trpv1 by nNOS and peroxynitrite as a key trigger of skeletal muscle hypertrophy. |
| 1813 | 23202294 | Here we show that neuronal nitric oxide synthase (nNOS) regulates load-induced hypertrophy by activating transient receptor potential cation channel, subfamily V, member 1 (TRPV1). |
| 1814 | 23443106 | Asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase (NOS) inhibitor, is known as mediator of endothelial cell dysfunction and atherosclerosis. |
| 1815 | 23523715 | Endothelium removal, PEG-catalase (hydrogen peroxide scavenger) or l-NPA (neuronal nitric oxide synthase, nNOS, inhibitor) increased angiotensin II-induced contraction in contralateral carotid from diabetic operated rats to the levels observed in diabetic non-operated rat carotid. |
| 1816 | 23523715 | Our findings suggest that carotid balloon injury in diabetic rats elicits a neurocompensation that attenuates the diabetic hyperreactivity to angiotensin II in contralateral carotid by a sensory nerves-dependent mechanism mediated by hydrogen peroxide derived from endothelial nNOS. |
| 1817 | 23523715 | Endothelium removal, PEG-catalase (hydrogen peroxide scavenger) or l-NPA (neuronal nitric oxide synthase, nNOS, inhibitor) increased angiotensin II-induced contraction in contralateral carotid from diabetic operated rats to the levels observed in diabetic non-operated rat carotid. |
| 1818 | 23523715 | Our findings suggest that carotid balloon injury in diabetic rats elicits a neurocompensation that attenuates the diabetic hyperreactivity to angiotensin II in contralateral carotid by a sensory nerves-dependent mechanism mediated by hydrogen peroxide derived from endothelial nNOS. |
| 1819 | 23585138 | We hypothesized that genetic eNOS deletion and 3-day nitric oxide synthase (NOS) inhibition in rodents would result in impaired mitochondrial biogenesis and defunct fission/fusion and autophagy profiles within the aorta. |
| 1820 | 23585138 | In response to NOS inhibition with NG-nitro-L-arginine methyl ester (L-NAME) treatment in Sprague Dawley rats, significant decreases were observed in ETC protein subunits from complexes I, III, and IV as well as voltage-dependent anion channel 1. |
| 1821 | 23585138 | Both genetic eNOS deletion and NOS inhibition resulted in decreased manganese superoxide dismutase protein. |
| 1822 | 23585138 | We hypothesized that genetic eNOS deletion and 3-day nitric oxide synthase (NOS) inhibition in rodents would result in impaired mitochondrial biogenesis and defunct fission/fusion and autophagy profiles within the aorta. |
| 1823 | 23585138 | In response to NOS inhibition with NG-nitro-L-arginine methyl ester (L-NAME) treatment in Sprague Dawley rats, significant decreases were observed in ETC protein subunits from complexes I, III, and IV as well as voltage-dependent anion channel 1. |
| 1824 | 23585138 | Both genetic eNOS deletion and NOS inhibition resulted in decreased manganese superoxide dismutase protein. |
| 1825 | 23585138 | We hypothesized that genetic eNOS deletion and 3-day nitric oxide synthase (NOS) inhibition in rodents would result in impaired mitochondrial biogenesis and defunct fission/fusion and autophagy profiles within the aorta. |
| 1826 | 23585138 | In response to NOS inhibition with NG-nitro-L-arginine methyl ester (L-NAME) treatment in Sprague Dawley rats, significant decreases were observed in ETC protein subunits from complexes I, III, and IV as well as voltage-dependent anion channel 1. |
| 1827 | 23585138 | Both genetic eNOS deletion and NOS inhibition resulted in decreased manganese superoxide dismutase protein. |
| 1828 | 23658158 | The nNOS-p38MAPK pathway is mediated by NOS1AP during neuronal death. |
| 1829 | 23658158 | Excitotoxic stimulus induces recruitment of NOS1AP to nNOS in rat cortical neuron culture. |
| 1830 | 23658158 | Excitotoxic activation of p38MAPK and subsequent neuronal death are reduced by competing with the nNOS:NOS1AP interaction and by knockdown with NOS1AP-targeting siRNAs. |
| 1831 | 23658158 | We designed a cell-permeable peptide that competes for the unique PDZ domain of nNOS that interacts with NOS1AP. |
| 1832 | 23658158 | This peptide inhibits NMDA-induced recruitment of NOS1AP to nNOS and in vivo in rat, doubles surviving tissue in a severe model of neonatal hypoxia-ischemia, a major cause of neonatal death and pediatric disability. |
| 1833 | 23658158 | The highly unusual sequence specificity of the nNOS:NOS1AP interaction and involvement in excitotoxic signaling may provide future opportunities for generation of neuroprotectants with high specificity. |
| 1834 | 23658158 | The nNOS-p38MAPK pathway is mediated by NOS1AP during neuronal death. |
| 1835 | 23658158 | Excitotoxic stimulus induces recruitment of NOS1AP to nNOS in rat cortical neuron culture. |
| 1836 | 23658158 | Excitotoxic activation of p38MAPK and subsequent neuronal death are reduced by competing with the nNOS:NOS1AP interaction and by knockdown with NOS1AP-targeting siRNAs. |
| 1837 | 23658158 | We designed a cell-permeable peptide that competes for the unique PDZ domain of nNOS that interacts with NOS1AP. |
| 1838 | 23658158 | This peptide inhibits NMDA-induced recruitment of NOS1AP to nNOS and in vivo in rat, doubles surviving tissue in a severe model of neonatal hypoxia-ischemia, a major cause of neonatal death and pediatric disability. |
| 1839 | 23658158 | The highly unusual sequence specificity of the nNOS:NOS1AP interaction and involvement in excitotoxic signaling may provide future opportunities for generation of neuroprotectants with high specificity. |
| 1840 | 23658158 | The nNOS-p38MAPK pathway is mediated by NOS1AP during neuronal death. |
| 1841 | 23658158 | Excitotoxic stimulus induces recruitment of NOS1AP to nNOS in rat cortical neuron culture. |
| 1842 | 23658158 | Excitotoxic activation of p38MAPK and subsequent neuronal death are reduced by competing with the nNOS:NOS1AP interaction and by knockdown with NOS1AP-targeting siRNAs. |
| 1843 | 23658158 | We designed a cell-permeable peptide that competes for the unique PDZ domain of nNOS that interacts with NOS1AP. |
| 1844 | 23658158 | This peptide inhibits NMDA-induced recruitment of NOS1AP to nNOS and in vivo in rat, doubles surviving tissue in a severe model of neonatal hypoxia-ischemia, a major cause of neonatal death and pediatric disability. |
| 1845 | 23658158 | The highly unusual sequence specificity of the nNOS:NOS1AP interaction and involvement in excitotoxic signaling may provide future opportunities for generation of neuroprotectants with high specificity. |
| 1846 | 23658158 | The nNOS-p38MAPK pathway is mediated by NOS1AP during neuronal death. |
| 1847 | 23658158 | Excitotoxic stimulus induces recruitment of NOS1AP to nNOS in rat cortical neuron culture. |
| 1848 | 23658158 | Excitotoxic activation of p38MAPK and subsequent neuronal death are reduced by competing with the nNOS:NOS1AP interaction and by knockdown with NOS1AP-targeting siRNAs. |
| 1849 | 23658158 | We designed a cell-permeable peptide that competes for the unique PDZ domain of nNOS that interacts with NOS1AP. |
| 1850 | 23658158 | This peptide inhibits NMDA-induced recruitment of NOS1AP to nNOS and in vivo in rat, doubles surviving tissue in a severe model of neonatal hypoxia-ischemia, a major cause of neonatal death and pediatric disability. |
| 1851 | 23658158 | The highly unusual sequence specificity of the nNOS:NOS1AP interaction and involvement in excitotoxic signaling may provide future opportunities for generation of neuroprotectants with high specificity. |
| 1852 | 23658158 | The nNOS-p38MAPK pathway is mediated by NOS1AP during neuronal death. |
| 1853 | 23658158 | Excitotoxic stimulus induces recruitment of NOS1AP to nNOS in rat cortical neuron culture. |
| 1854 | 23658158 | Excitotoxic activation of p38MAPK and subsequent neuronal death are reduced by competing with the nNOS:NOS1AP interaction and by knockdown with NOS1AP-targeting siRNAs. |
| 1855 | 23658158 | We designed a cell-permeable peptide that competes for the unique PDZ domain of nNOS that interacts with NOS1AP. |
| 1856 | 23658158 | This peptide inhibits NMDA-induced recruitment of NOS1AP to nNOS and in vivo in rat, doubles surviving tissue in a severe model of neonatal hypoxia-ischemia, a major cause of neonatal death and pediatric disability. |
| 1857 | 23658158 | The highly unusual sequence specificity of the nNOS:NOS1AP interaction and involvement in excitotoxic signaling may provide future opportunities for generation of neuroprotectants with high specificity. |
| 1858 | 23658158 | The nNOS-p38MAPK pathway is mediated by NOS1AP during neuronal death. |
| 1859 | 23658158 | Excitotoxic stimulus induces recruitment of NOS1AP to nNOS in rat cortical neuron culture. |
| 1860 | 23658158 | Excitotoxic activation of p38MAPK and subsequent neuronal death are reduced by competing with the nNOS:NOS1AP interaction and by knockdown with NOS1AP-targeting siRNAs. |
| 1861 | 23658158 | We designed a cell-permeable peptide that competes for the unique PDZ domain of nNOS that interacts with NOS1AP. |
| 1862 | 23658158 | This peptide inhibits NMDA-induced recruitment of NOS1AP to nNOS and in vivo in rat, doubles surviving tissue in a severe model of neonatal hypoxia-ischemia, a major cause of neonatal death and pediatric disability. |
| 1863 | 23658158 | The highly unusual sequence specificity of the nNOS:NOS1AP interaction and involvement in excitotoxic signaling may provide future opportunities for generation of neuroprotectants with high specificity. |
| 1864 | 23680665 | Neuronal nitric oxide synthase is phosphorylated in response to insulin stimulation in skeletal muscle. |
| 1865 | 23680665 | Reduced insulin sensitivity has been associated with reduced nitric oxide synthase (NOS) activity and impaired glucose uptake in T2DM skeletal muscle. |
| 1866 | 23680665 | Neuronal NOS (nNOS), the primary NOS isoform in skeletal muscle, contains a homologous phosphorylation site, raising the possibility that nNOS, too, may undergo an activating phosphorylation event upon insulin treatment. |
| 1867 | 23680665 | Yet it remains unknown if or how nNOS is regulated by insulin in skeletal muscle. |
| 1868 | 23680665 | Data shown herein indicate that nNOS is phosphorylated in response to insulin in skeletal muscle and that this phosphorylation event occurs rapidly in C2C12 myotubes, resulting in increased NO production. |
| 1869 | 23680665 | In vivo phosphorylation of nNOS was also observed in response to insulin in mouse skeletal muscle. |
| 1870 | 23680665 | These results indicate, for the first time, that nNOS is phosphorylated in skeletal muscle in response to insulin and in association with increased NO production. |
| 1871 | 23680665 | Neuronal nitric oxide synthase is phosphorylated in response to insulin stimulation in skeletal muscle. |
| 1872 | 23680665 | Reduced insulin sensitivity has been associated with reduced nitric oxide synthase (NOS) activity and impaired glucose uptake in T2DM skeletal muscle. |
| 1873 | 23680665 | Neuronal NOS (nNOS), the primary NOS isoform in skeletal muscle, contains a homologous phosphorylation site, raising the possibility that nNOS, too, may undergo an activating phosphorylation event upon insulin treatment. |
| 1874 | 23680665 | Yet it remains unknown if or how nNOS is regulated by insulin in skeletal muscle. |
| 1875 | 23680665 | Data shown herein indicate that nNOS is phosphorylated in response to insulin in skeletal muscle and that this phosphorylation event occurs rapidly in C2C12 myotubes, resulting in increased NO production. |
| 1876 | 23680665 | In vivo phosphorylation of nNOS was also observed in response to insulin in mouse skeletal muscle. |
| 1877 | 23680665 | These results indicate, for the first time, that nNOS is phosphorylated in skeletal muscle in response to insulin and in association with increased NO production. |
| 1878 | 23680665 | Neuronal nitric oxide synthase is phosphorylated in response to insulin stimulation in skeletal muscle. |
| 1879 | 23680665 | Reduced insulin sensitivity has been associated with reduced nitric oxide synthase (NOS) activity and impaired glucose uptake in T2DM skeletal muscle. |
| 1880 | 23680665 | Neuronal NOS (nNOS), the primary NOS isoform in skeletal muscle, contains a homologous phosphorylation site, raising the possibility that nNOS, too, may undergo an activating phosphorylation event upon insulin treatment. |
| 1881 | 23680665 | Yet it remains unknown if or how nNOS is regulated by insulin in skeletal muscle. |
| 1882 | 23680665 | Data shown herein indicate that nNOS is phosphorylated in response to insulin in skeletal muscle and that this phosphorylation event occurs rapidly in C2C12 myotubes, resulting in increased NO production. |
| 1883 | 23680665 | In vivo phosphorylation of nNOS was also observed in response to insulin in mouse skeletal muscle. |
| 1884 | 23680665 | These results indicate, for the first time, that nNOS is phosphorylated in skeletal muscle in response to insulin and in association with increased NO production. |
| 1885 | 23680665 | Neuronal nitric oxide synthase is phosphorylated in response to insulin stimulation in skeletal muscle. |
| 1886 | 23680665 | Reduced insulin sensitivity has been associated with reduced nitric oxide synthase (NOS) activity and impaired glucose uptake in T2DM skeletal muscle. |
| 1887 | 23680665 | Neuronal NOS (nNOS), the primary NOS isoform in skeletal muscle, contains a homologous phosphorylation site, raising the possibility that nNOS, too, may undergo an activating phosphorylation event upon insulin treatment. |
| 1888 | 23680665 | Yet it remains unknown if or how nNOS is regulated by insulin in skeletal muscle. |
| 1889 | 23680665 | Data shown herein indicate that nNOS is phosphorylated in response to insulin in skeletal muscle and that this phosphorylation event occurs rapidly in C2C12 myotubes, resulting in increased NO production. |
| 1890 | 23680665 | In vivo phosphorylation of nNOS was also observed in response to insulin in mouse skeletal muscle. |
| 1891 | 23680665 | These results indicate, for the first time, that nNOS is phosphorylated in skeletal muscle in response to insulin and in association with increased NO production. |
| 1892 | 23680665 | Neuronal nitric oxide synthase is phosphorylated in response to insulin stimulation in skeletal muscle. |
| 1893 | 23680665 | Reduced insulin sensitivity has been associated with reduced nitric oxide synthase (NOS) activity and impaired glucose uptake in T2DM skeletal muscle. |
| 1894 | 23680665 | Neuronal NOS (nNOS), the primary NOS isoform in skeletal muscle, contains a homologous phosphorylation site, raising the possibility that nNOS, too, may undergo an activating phosphorylation event upon insulin treatment. |
| 1895 | 23680665 | Yet it remains unknown if or how nNOS is regulated by insulin in skeletal muscle. |
| 1896 | 23680665 | Data shown herein indicate that nNOS is phosphorylated in response to insulin in skeletal muscle and that this phosphorylation event occurs rapidly in C2C12 myotubes, resulting in increased NO production. |
| 1897 | 23680665 | In vivo phosphorylation of nNOS was also observed in response to insulin in mouse skeletal muscle. |
| 1898 | 23680665 | These results indicate, for the first time, that nNOS is phosphorylated in skeletal muscle in response to insulin and in association with increased NO production. |
| 1899 | 23680665 | Neuronal nitric oxide synthase is phosphorylated in response to insulin stimulation in skeletal muscle. |
| 1900 | 23680665 | Reduced insulin sensitivity has been associated with reduced nitric oxide synthase (NOS) activity and impaired glucose uptake in T2DM skeletal muscle. |
| 1901 | 23680665 | Neuronal NOS (nNOS), the primary NOS isoform in skeletal muscle, contains a homologous phosphorylation site, raising the possibility that nNOS, too, may undergo an activating phosphorylation event upon insulin treatment. |
| 1902 | 23680665 | Yet it remains unknown if or how nNOS is regulated by insulin in skeletal muscle. |
| 1903 | 23680665 | Data shown herein indicate that nNOS is phosphorylated in response to insulin in skeletal muscle and that this phosphorylation event occurs rapidly in C2C12 myotubes, resulting in increased NO production. |
| 1904 | 23680665 | In vivo phosphorylation of nNOS was also observed in response to insulin in mouse skeletal muscle. |
| 1905 | 23680665 | These results indicate, for the first time, that nNOS is phosphorylated in skeletal muscle in response to insulin and in association with increased NO production. |
| 1906 | 23680665 | Neuronal nitric oxide synthase is phosphorylated in response to insulin stimulation in skeletal muscle. |
| 1907 | 23680665 | Reduced insulin sensitivity has been associated with reduced nitric oxide synthase (NOS) activity and impaired glucose uptake in T2DM skeletal muscle. |
| 1908 | 23680665 | Neuronal NOS (nNOS), the primary NOS isoform in skeletal muscle, contains a homologous phosphorylation site, raising the possibility that nNOS, too, may undergo an activating phosphorylation event upon insulin treatment. |
| 1909 | 23680665 | Yet it remains unknown if or how nNOS is regulated by insulin in skeletal muscle. |
| 1910 | 23680665 | Data shown herein indicate that nNOS is phosphorylated in response to insulin in skeletal muscle and that this phosphorylation event occurs rapidly in C2C12 myotubes, resulting in increased NO production. |
| 1911 | 23680665 | In vivo phosphorylation of nNOS was also observed in response to insulin in mouse skeletal muscle. |
| 1912 | 23680665 | These results indicate, for the first time, that nNOS is phosphorylated in skeletal muscle in response to insulin and in association with increased NO production. |
| 1913 | 23702602 | The association of adipose-derived dimethylarginine dimethylaminohydrolase-2 with insulin sensitivity in experimental type 2 diabetes mellitus. |
| 1914 | 23702602 | Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthase (NOS), which can be hydrolyzed by dimethylarginine-dimethylaminohydrolase (DDAH). |
| 1915 | 23702602 | In the present study, we examined the effects of adipocyte-derived DDAH/ADMA on insulin sensitivity using animal and cell models. |
| 1916 | 23702602 | Results showed that in adipose tissue of high fat diet-fed diabetic rats, as well as in high glucose (25 mM) plus insulin (100 nM)-treated 3T3-L1 adipocytes, expression levels of insulin receptor substance-1 (IRS-1), glucose transporter-4 (GLUT-4), and DDAH isoform-2 (DDAH-2) were down-regulated compared with control, although DDAH-1 expression showed no significant changes. |
| 1917 | 23702602 | We also observed that nitric oxide bioavailability, DDAH and NOS activities were subsequently decreased, while the local ADMA content was elevated in diabetic adipose tissue. |
| 1918 | 23702602 | Transfection of human DDAH-2 gene into high glucose- and insulin-treated 3T3-L1 adipocytes significantly ameliorated DDAH activity, reduced ADMA contents, and up-regulated the mRNA expression levels of IRS-1 and GLUT-4. |
| 1919 | 23702602 | These findings suggested that in the development of type 2 diabetes mellitus, local DDAH-2 in adipocytes might play an important role in regulating insulin sensitivity. |
| 1920 | 23702602 | The association of adipose-derived dimethylarginine dimethylaminohydrolase-2 with insulin sensitivity in experimental type 2 diabetes mellitus. |
| 1921 | 23702602 | Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthase (NOS), which can be hydrolyzed by dimethylarginine-dimethylaminohydrolase (DDAH). |
| 1922 | 23702602 | In the present study, we examined the effects of adipocyte-derived DDAH/ADMA on insulin sensitivity using animal and cell models. |
| 1923 | 23702602 | Results showed that in adipose tissue of high fat diet-fed diabetic rats, as well as in high glucose (25 mM) plus insulin (100 nM)-treated 3T3-L1 adipocytes, expression levels of insulin receptor substance-1 (IRS-1), glucose transporter-4 (GLUT-4), and DDAH isoform-2 (DDAH-2) were down-regulated compared with control, although DDAH-1 expression showed no significant changes. |
| 1924 | 23702602 | We also observed that nitric oxide bioavailability, DDAH and NOS activities were subsequently decreased, while the local ADMA content was elevated in diabetic adipose tissue. |
| 1925 | 23702602 | Transfection of human DDAH-2 gene into high glucose- and insulin-treated 3T3-L1 adipocytes significantly ameliorated DDAH activity, reduced ADMA contents, and up-regulated the mRNA expression levels of IRS-1 and GLUT-4. |
| 1926 | 23702602 | These findings suggested that in the development of type 2 diabetes mellitus, local DDAH-2 in adipocytes might play an important role in regulating insulin sensitivity. |
| 1927 | 23820268 | Folic acid reverses nitric oxide synthase uncoupling and prevents cardiac dysfunction in insulin resistance: role of Ca2+/calmodulin-activated protein kinase II. |
| 1928 | 23820268 | Nitric oxide synthase (NOS) may be uncoupled to produce superoxide rather than nitric oxide (NO) under pathological conditions such as diabetes mellitus and insulin resistance, leading to cardiac contractile anomalies. |
| 1929 | 23820268 | Nonetheless, the role of NOS uncoupling in insulin resistance-induced cardiac dysfunction remains elusive. |
| 1930 | 23820268 | Given that folic acid may produce beneficial effects for cardiac insufficiency partially through its NOS recoupling capacity, this study was designed to evaluate the effect of folic acid on insulin resistance-induced cardiac contractile dysfunction in a sucrose-induced insulin resistance model. |
| 1931 | 23820268 | Our results revealed whole body insulin resistance after sucrose feeding associated with diminished NO production, elevated peroxynitrite (ONOO(-)) levels, and impaired echocardiographic and cardiomyocyte function along with a leaky ryanodine receptor (RYR) and intracellular Ca(2+) handling derangement. |
| 1932 | 23820268 | Western blot analysis showed that insulin resistance significantly promoted Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) phosphorylation, which might be responsible for the leaky RYR and cardiac mechanical dysfunction. |
| 1933 | 23820268 | NOS recoupling using folic acid reversed insulin resistance-induced changes in NO and ONOO(-), CaMKII phosphorylation, and cardiac mechanical abnormalities. |
| 1934 | 23820268 | Taken together, these data demonstrated that treatment with folic acid may reverse cardiac contractile and intracellular Ca(2+) anomalies through ablation of CaMKII phosphorylation and RYR Ca(2+) leak. |
| 1935 | 23820268 | Folic acid reverses nitric oxide synthase uncoupling and prevents cardiac dysfunction in insulin resistance: role of Ca2+/calmodulin-activated protein kinase II. |
| 1936 | 23820268 | Nitric oxide synthase (NOS) may be uncoupled to produce superoxide rather than nitric oxide (NO) under pathological conditions such as diabetes mellitus and insulin resistance, leading to cardiac contractile anomalies. |
| 1937 | 23820268 | Nonetheless, the role of NOS uncoupling in insulin resistance-induced cardiac dysfunction remains elusive. |
| 1938 | 23820268 | Given that folic acid may produce beneficial effects for cardiac insufficiency partially through its NOS recoupling capacity, this study was designed to evaluate the effect of folic acid on insulin resistance-induced cardiac contractile dysfunction in a sucrose-induced insulin resistance model. |
| 1939 | 23820268 | Our results revealed whole body insulin resistance after sucrose feeding associated with diminished NO production, elevated peroxynitrite (ONOO(-)) levels, and impaired echocardiographic and cardiomyocyte function along with a leaky ryanodine receptor (RYR) and intracellular Ca(2+) handling derangement. |
| 1940 | 23820268 | Western blot analysis showed that insulin resistance significantly promoted Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) phosphorylation, which might be responsible for the leaky RYR and cardiac mechanical dysfunction. |
| 1941 | 23820268 | NOS recoupling using folic acid reversed insulin resistance-induced changes in NO and ONOO(-), CaMKII phosphorylation, and cardiac mechanical abnormalities. |
| 1942 | 23820268 | Taken together, these data demonstrated that treatment with folic acid may reverse cardiac contractile and intracellular Ca(2+) anomalies through ablation of CaMKII phosphorylation and RYR Ca(2+) leak. |
| 1943 | 23820268 | Folic acid reverses nitric oxide synthase uncoupling and prevents cardiac dysfunction in insulin resistance: role of Ca2+/calmodulin-activated protein kinase II. |
| 1944 | 23820268 | Nitric oxide synthase (NOS) may be uncoupled to produce superoxide rather than nitric oxide (NO) under pathological conditions such as diabetes mellitus and insulin resistance, leading to cardiac contractile anomalies. |
| 1945 | 23820268 | Nonetheless, the role of NOS uncoupling in insulin resistance-induced cardiac dysfunction remains elusive. |
| 1946 | 23820268 | Given that folic acid may produce beneficial effects for cardiac insufficiency partially through its NOS recoupling capacity, this study was designed to evaluate the effect of folic acid on insulin resistance-induced cardiac contractile dysfunction in a sucrose-induced insulin resistance model. |
| 1947 | 23820268 | Our results revealed whole body insulin resistance after sucrose feeding associated with diminished NO production, elevated peroxynitrite (ONOO(-)) levels, and impaired echocardiographic and cardiomyocyte function along with a leaky ryanodine receptor (RYR) and intracellular Ca(2+) handling derangement. |
| 1948 | 23820268 | Western blot analysis showed that insulin resistance significantly promoted Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) phosphorylation, which might be responsible for the leaky RYR and cardiac mechanical dysfunction. |
| 1949 | 23820268 | NOS recoupling using folic acid reversed insulin resistance-induced changes in NO and ONOO(-), CaMKII phosphorylation, and cardiac mechanical abnormalities. |
| 1950 | 23820268 | Taken together, these data demonstrated that treatment with folic acid may reverse cardiac contractile and intracellular Ca(2+) anomalies through ablation of CaMKII phosphorylation and RYR Ca(2+) leak. |
| 1951 | 23820268 | Folic acid reverses nitric oxide synthase uncoupling and prevents cardiac dysfunction in insulin resistance: role of Ca2+/calmodulin-activated protein kinase II. |
| 1952 | 23820268 | Nitric oxide synthase (NOS) may be uncoupled to produce superoxide rather than nitric oxide (NO) under pathological conditions such as diabetes mellitus and insulin resistance, leading to cardiac contractile anomalies. |
| 1953 | 23820268 | Nonetheless, the role of NOS uncoupling in insulin resistance-induced cardiac dysfunction remains elusive. |
| 1954 | 23820268 | Given that folic acid may produce beneficial effects for cardiac insufficiency partially through its NOS recoupling capacity, this study was designed to evaluate the effect of folic acid on insulin resistance-induced cardiac contractile dysfunction in a sucrose-induced insulin resistance model. |
| 1955 | 23820268 | Our results revealed whole body insulin resistance after sucrose feeding associated with diminished NO production, elevated peroxynitrite (ONOO(-)) levels, and impaired echocardiographic and cardiomyocyte function along with a leaky ryanodine receptor (RYR) and intracellular Ca(2+) handling derangement. |
| 1956 | 23820268 | Western blot analysis showed that insulin resistance significantly promoted Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) phosphorylation, which might be responsible for the leaky RYR and cardiac mechanical dysfunction. |
| 1957 | 23820268 | NOS recoupling using folic acid reversed insulin resistance-induced changes in NO and ONOO(-), CaMKII phosphorylation, and cardiac mechanical abnormalities. |
| 1958 | 23820268 | Taken together, these data demonstrated that treatment with folic acid may reverse cardiac contractile and intracellular Ca(2+) anomalies through ablation of CaMKII phosphorylation and RYR Ca(2+) leak. |
| 1959 | 23848484 | The expressions of endothelial nitric oxide synthase (eNOS), phosphorylated eNOS (p-eNOS) (Ser-1177), neuronal nitric oxide synthase (nNOS), NADPH oxidase subunit gp91(phox) , Rho A, and Rho kinase in corpus cavernosum were semi-quantitatively assessed by immunohistochemistry. |
| 1960 | 23848484 | Furthermore, eNOS, p-eNOS, and nNOS expressions decreased significantly in diabetic rats compared to controls, while gp91(phox) , RhoA and Rho kinase expressions increased significantly. |
| 1961 | 23848484 | The expressions of endothelial nitric oxide synthase (eNOS), phosphorylated eNOS (p-eNOS) (Ser-1177), neuronal nitric oxide synthase (nNOS), NADPH oxidase subunit gp91(phox) , Rho A, and Rho kinase in corpus cavernosum were semi-quantitatively assessed by immunohistochemistry. |
| 1962 | 23848484 | Furthermore, eNOS, p-eNOS, and nNOS expressions decreased significantly in diabetic rats compared to controls, while gp91(phox) , RhoA and Rho kinase expressions increased significantly. |
| 1963 | 23859953 | Nitric oxide (NO) is synthetized enzymatically from l-arginine (l-Arg) by three NO synthase isoforms, iNOS, eNOS and nNOS. |
| 1964 | 23881404 | High-fat diet ingestion correlated with a loss of neurons expressing VIP and nNOS but did not affect the expression of ChAT, substance P, calbindin and CGRP. |