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Gene Information
Gene symbol: TAC1
Gene name: tachykinin, precursor 1
HGNC ID: 11517
Synonyms: NPK
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 44799 | The different mode of secretion of the gut hormones (paracrine secretion--somatostatin. endocrine and neurocrine secretion--gastrin, CCK; neurocrine secretion--VIP, substance P), obscures the physiological significance of these hormones. |
| 2 | 814025 | The effects of thyrotropin-releasing hormone, luteinizing hormone-releasing hormone, substance P, somatostatin, and a partially purified hypothalamic extract on insulin secretion were tested both in vitro and in vivo. |
| 3 | 814025 | Only somatostatin and the hypothalamic extract affected insulin secretion. |
| 4 | 814025 | In vitro, somatostatin decreased glucose-stimulated insulin secretion by isolated islets and in vivo significantly reduced the rate of insulin output into the portal vein. |
| 5 | 1310640 | Receptors for vasoactive intestinal peptide (VIP) and muscarinic cholinergic agents occurred on 60%, bombesin and gastrin on 30%, beta-adrenergic agents and gastrin-releasing peptide (GRP) on 20%, and somatostatin, opiates, neuromedin B, and substance P on 10%. |
| 6 | 1310640 | Inhibition of binding by agonists revealed relative potencies of 125I-[Tyr4]bombesin greater than GRP much greater than neuromedin B, and two recently described antagonists were similar in potency to GRP. |
| 7 | 1310640 | These results demonstrate the presence of several different receptors for gastrointestinal hormones or neurotransmitters, some described for the first time, on human colon cancer cell lines, including bombesin-related peptides, VIP, somatostatin, substance P, beta-adrenergic agents, calcitonin gene-related peptide, gastrin, muscarinic cholinergic agents, and opiates. |
| 8 | 1310640 | Receptors for vasoactive intestinal peptide (VIP) and muscarinic cholinergic agents occurred on 60%, bombesin and gastrin on 30%, beta-adrenergic agents and gastrin-releasing peptide (GRP) on 20%, and somatostatin, opiates, neuromedin B, and substance P on 10%. |
| 9 | 1310640 | Inhibition of binding by agonists revealed relative potencies of 125I-[Tyr4]bombesin greater than GRP much greater than neuromedin B, and two recently described antagonists were similar in potency to GRP. |
| 10 | 1310640 | These results demonstrate the presence of several different receptors for gastrointestinal hormones or neurotransmitters, some described for the first time, on human colon cancer cell lines, including bombesin-related peptides, VIP, somatostatin, substance P, beta-adrenergic agents, calcitonin gene-related peptide, gastrin, muscarinic cholinergic agents, and opiates. |
| 11 | 1329527 | (R)-p-cAMPS had no effect on contraction stimulated by carbachol, cholecystokinin, or substance P. |
| 12 | 1329527 | These data demonstrate that activation of protein kinase A is primarily responsible for mediating gastrin smooth muscle relaxation produced by adrenergic agents and various neuropeptides. |
| 13 | 1346384 | Six, 8, 14, or 20-21 wk after transplantation, the graft-bearing kidney was removed and processed for microscopical examinations with indirect immunofluorescence for neuropeptides and tyrosine hydroxylase, and with acetylcholinesterase staining to visualize nerve fibers within the graft. |
| 14 | 1346384 | The findings demonstrate the presence of sympathetic nerve fibers (containing tyrosine hydroxylase and neuropeptide Y), mainly accompanying ingrowing blood vessels; parasympathetic nerve fibers (containing acetylcholinesterase and vasoactive intestinal peptide), possibly reaching the graft from the adjacent renal capsule; and afferent nerve fibers (containing substance P and calcitonin gene-related peptide), which were less numerous. |
| 15 | 1374869 | Depletion of substance P and calcitonin gene-related peptide in sciatic nerve of rats with experimental diabetes; effects of insulin and aldose reductase inhibition. |
| 16 | 1374869 | This study was designed to determine whether deficient substance P in the sciatic nerve of diabetic rats was associated with a similar reduction in calcitonin gene-related peptide and whether the depletion of either or both peptides could be affected by insulin treatment or by aldose reductase inhibition. |
| 17 | 1374869 | Tight glycaemic control with insulin prevented completely the deficit in both peptides (substance P = 0.096 +/- 0.021, calcitonin gene-related peptide = 4.66 +/- 0.92). |
| 18 | 1374869 | Treatment with the aldose reductase inhibitor, imirestat, corrected the substance P deficit (0.08 +/- 0.018) and attenuated the calcitonin gene-related peptide (3.55 +/- 1.03) depletion seen in the untreated diabetic animals. |
| 19 | 1374869 | Depletion of substance P and calcitonin gene-related peptide in sciatic nerve of rats with experimental diabetes; effects of insulin and aldose reductase inhibition. |
| 20 | 1374869 | This study was designed to determine whether deficient substance P in the sciatic nerve of diabetic rats was associated with a similar reduction in calcitonin gene-related peptide and whether the depletion of either or both peptides could be affected by insulin treatment or by aldose reductase inhibition. |
| 21 | 1374869 | Tight glycaemic control with insulin prevented completely the deficit in both peptides (substance P = 0.096 +/- 0.021, calcitonin gene-related peptide = 4.66 +/- 0.92). |
| 22 | 1374869 | Treatment with the aldose reductase inhibitor, imirestat, corrected the substance P deficit (0.08 +/- 0.018) and attenuated the calcitonin gene-related peptide (3.55 +/- 1.03) depletion seen in the untreated diabetic animals. |
| 23 | 1374869 | Depletion of substance P and calcitonin gene-related peptide in sciatic nerve of rats with experimental diabetes; effects of insulin and aldose reductase inhibition. |
| 24 | 1374869 | This study was designed to determine whether deficient substance P in the sciatic nerve of diabetic rats was associated with a similar reduction in calcitonin gene-related peptide and whether the depletion of either or both peptides could be affected by insulin treatment or by aldose reductase inhibition. |
| 25 | 1374869 | Tight glycaemic control with insulin prevented completely the deficit in both peptides (substance P = 0.096 +/- 0.021, calcitonin gene-related peptide = 4.66 +/- 0.92). |
| 26 | 1374869 | Treatment with the aldose reductase inhibitor, imirestat, corrected the substance P deficit (0.08 +/- 0.018) and attenuated the calcitonin gene-related peptide (3.55 +/- 1.03) depletion seen in the untreated diabetic animals. |
| 27 | 1374869 | Depletion of substance P and calcitonin gene-related peptide in sciatic nerve of rats with experimental diabetes; effects of insulin and aldose reductase inhibition. |
| 28 | 1374869 | This study was designed to determine whether deficient substance P in the sciatic nerve of diabetic rats was associated with a similar reduction in calcitonin gene-related peptide and whether the depletion of either or both peptides could be affected by insulin treatment or by aldose reductase inhibition. |
| 29 | 1374869 | Tight glycaemic control with insulin prevented completely the deficit in both peptides (substance P = 0.096 +/- 0.021, calcitonin gene-related peptide = 4.66 +/- 0.92). |
| 30 | 1374869 | Treatment with the aldose reductase inhibitor, imirestat, corrected the substance P deficit (0.08 +/- 0.018) and attenuated the calcitonin gene-related peptide (3.55 +/- 1.03) depletion seen in the untreated diabetic animals. |
| 31 | 1379366 | In a previous study, we found that first incubating guinea pig pancreatic acini with carbachol caused desensitization of the enzyme secretory response to cholecystokinin-octapeptide (CCK-8), bombesin, and carbachol but not that to substance P. |
| 32 | 1379366 | First incubating pancreatic acini with carbachol did not alter either substance P-stimulated enzyme secretion or binding of 125I-substance P to substance P receptors, whereas in the same experiments, carbachol reduced binding of 125I-CCK-8 to cholecystokinin receptors by 50% and decreased in CCK-8-stimulated enzyme secretion by 50%. |
| 33 | 1379366 | In a previous study, we found that first incubating guinea pig pancreatic acini with carbachol caused desensitization of the enzyme secretory response to cholecystokinin-octapeptide (CCK-8), bombesin, and carbachol but not that to substance P. |
| 34 | 1379366 | First incubating pancreatic acini with carbachol did not alter either substance P-stimulated enzyme secretion or binding of 125I-substance P to substance P receptors, whereas in the same experiments, carbachol reduced binding of 125I-CCK-8 to cholecystokinin receptors by 50% and decreased in CCK-8-stimulated enzyme secretion by 50%. |
| 35 | 1380399 | Immunohistochemical characterization of NPY and substance P containing nerve terminals in aged and diabetic human sympathetic ganglia. |
| 36 | 1380399 | To compare the neuropeptide specificity of dystrophic axon formation in aging versus diabetic human sympathetic ganglia we have immunohistochemically characterized neuropeptide Y (NPY) and substance P containing intraganglionic nerve terminals. |
| 37 | 1380399 | Immunohistochemical characterization of NPY and substance P containing nerve terminals in aged and diabetic human sympathetic ganglia. |
| 38 | 1380399 | To compare the neuropeptide specificity of dystrophic axon formation in aging versus diabetic human sympathetic ganglia we have immunohistochemically characterized neuropeptide Y (NPY) and substance P containing intraganglionic nerve terminals. |
| 39 | 1435393 | Salivary glands express a variety of cell-surface receptors including adrenergic (alpha and beta), muscarinic-cholinergic, substance P, vasoactive intestinal peptide hormone, and ATP receptors. |
| 40 | 1587998 | There was no difference in dilator effect of acetylcholine and substance P between the diabetic animals and the control group in any of the vessel types, indicating that the changed vascular responses to NPY and noradrenaline were not endothelium-dependent. |
| 41 | 1638409 | Immunoassay of NPY confirmed increased levels in optic nerve sheaths and showed that substance P and calcitonin gene-related peptide levels increased in sciatic but not optic nerve sheaths. |
| 42 | 1675174 | Using quantification by image analysis and double-labeling immunohistochemistry on mesenteric veins, significant reductions in the density of nerve plexuses staining for 5-hydroxytryptamine (5-HT) and tyrosine hydroxylase (TH) were shown in vessels from diabetic rats compared to controls. |
| 43 | 1675174 | No reductions were observed in the density of nerve plexuses stained for the neuronal marker, PGP 9.5, or for substance P (SP), a marker for afferent nerve fibers. |
| 44 | 1689117 | First incubating guinea pig pancreatic acini with carbachol reduced the subsequent stimulation of amylase release caused by carbachol, cholecystokinin octapeptide (CCK-8), and bombesin but not that caused by vasoactive intestinal peptide, substance P, 8-bromoadenosine 3',5'-cyclic monophosphate, A23187, or 12-O-tetradecanoylphorbol-13-acetate. |
| 45 | 1689117 | Acini possess a single class of bombesin receptors, and first incubating acini with carbachol caused a 40% decrease in the number of bombesin receptors with no change in their affinity for bombesin. 12-O-tetradecanoyl phorbol-13-acetate reproduced the action of carbachol on binding of N-[3H]methylscopolamine and 125I-CCK-8 but not on binding of 125I-[Tyr4]bombesin, suggesting that carbachol activation of protein kinase C may in some way mediate the effect of carbachol on receptors for carbachol and those for CCK but not that on receptors for bombesin. |
| 46 | 1692544 | There was an increase in the intensity of immunoreactivity in vasoactive intestinal polypeptide- and neuropeptide Y-like immunoreactive nerve fibers and neurons and a decrease in calcitonin gene-related peptide-like immunoreactivity but no change in substance P- and dopamine beta-hydroxylase-like immunoreactivity in the nerve fibers and neurons of the submucous plexus of both 8- and 16-wk streptozocin-diabetic rat ileum. |
| 47 | 1692544 | However, in the myenteric plexus of the diabetic rat ileum, there was enlargement of varicosities and an increase followed by a slight decrease in the intensity of immunoreactivity of vasoactive intestinal polypeptide- and dopamine beta-hydroxylase-like immunoreactive nerve fibers and neurons, increased substance P-like immunoreactivity in diabetes at 16 wk, and an initial decrease (at 8 wk) followed by a recovery of calcitonin gene-related peptide-like immunoreactivity at 16 wk, but no change in neuropeptide Y-like immunoreactivity. |
| 48 | 1692544 | There was an increase in the intensity of immunoreactivity in vasoactive intestinal polypeptide- and neuropeptide Y-like immunoreactive nerve fibers and neurons and a decrease in calcitonin gene-related peptide-like immunoreactivity but no change in substance P- and dopamine beta-hydroxylase-like immunoreactivity in the nerve fibers and neurons of the submucous plexus of both 8- and 16-wk streptozocin-diabetic rat ileum. |
| 49 | 1692544 | However, in the myenteric plexus of the diabetic rat ileum, there was enlargement of varicosities and an increase followed by a slight decrease in the intensity of immunoreactivity of vasoactive intestinal polypeptide- and dopamine beta-hydroxylase-like immunoreactive nerve fibers and neurons, increased substance P-like immunoreactivity in diabetes at 16 wk, and an initial decrease (at 8 wk) followed by a recovery of calcitonin gene-related peptide-like immunoreactivity at 16 wk, but no change in neuropeptide Y-like immunoreactivity. |
| 50 | 1702423 | Recently, reduced peptide bond (psi) analogues of bombesin or substance P in which the -CONH- bond is replaced by -CH2NH- are reported to be receptor antagonists. |
| 51 | 1702423 | [psi 4,5]Secretin did not interact with cholecystokinin, bombesin, calcitonin gene-related peptide, or cholinergic receptors but did interact with receptors for vasoactive intestinal peptide, causing half-maximal inhibition at 72 microM and thus had a 18-fold higher affinity for secretin than vasoactive intestinal peptide receptors. |
| 52 | 1704001 | Skin samples dissected from the lip and footpad of diabetic rats, 2, 4, 8 and 12 weeks after streptozotocin injection and age matched controls were sectioned and were immunostained with antisera to the neuropeptides substance P, calcitonin gene-related peptide (CGRP), vasoactive intestinal polypeptide (VIP) and neuropeptide Y (NPY), and to a general neural marker, protein gene product 9.5 (PGP 9.5). |
| 53 | 1704001 | No differences were detected in nerves immunoreactive for either substance P in the epidermis and dermis, and NPY around blood vessels. |
| 54 | 1704001 | Skin samples dissected from the lip and footpad of diabetic rats, 2, 4, 8 and 12 weeks after streptozotocin injection and age matched controls were sectioned and were immunostained with antisera to the neuropeptides substance P, calcitonin gene-related peptide (CGRP), vasoactive intestinal polypeptide (VIP) and neuropeptide Y (NPY), and to a general neural marker, protein gene product 9.5 (PGP 9.5). |
| 55 | 1704001 | No differences were detected in nerves immunoreactive for either substance P in the epidermis and dermis, and NPY around blood vessels. |
| 56 | 1708136 | CGRP(32-37)-stimulated amylase release was not inhibited by the substance P receptor antagonist, spantide, by the bombesin receptor antagonist, [D-Phe6]bombesin(6-13) propylamide, or by the muscarinic receptor antagonist, atropine, but was inhibited by the CCK receptor antagonist L364,718. |
| 57 | 1719570 | These data suggest that STZ-induced diabetes selectively alters a neuronal system that involves substance P but not somatostatin in the spinal cord. |
| 58 | 1720364 | In female cp/cp rats, central hypothalamic levels of neuropeptide Y (NPY), neurotensin, somatostatin and substance P were significantly lower (p less than 0.02) than in lean female controls. |
| 59 | 1720364 | The other 4 peptides examined (bombesin, calcitonin gene-related peptide, neuromedin B and vasoactive intestinal peptide) did not differ significantly between cp/cp and lean females, either fed freely or food-restricted. |
| 60 | 1720364 | NPY and galanin are powerful and specific central appetite stimulants, whereas neurotensin, substance P and somatostatin inhibit feeding when injected centrally. |
| 61 | 1720364 | In female cp/cp rats, central hypothalamic levels of neuropeptide Y (NPY), neurotensin, somatostatin and substance P were significantly lower (p less than 0.02) than in lean female controls. |
| 62 | 1720364 | The other 4 peptides examined (bombesin, calcitonin gene-related peptide, neuromedin B and vasoactive intestinal peptide) did not differ significantly between cp/cp and lean females, either fed freely or food-restricted. |
| 63 | 1720364 | NPY and galanin are powerful and specific central appetite stimulants, whereas neurotensin, substance P and somatostatin inhibit feeding when injected centrally. |
| 64 | 1720876 | Changes of substance P and somatostatin contents in the gastrointestinal tract of streptozotocin diabetic rats. |
| 65 | 1720876 | Substance P and somatostatin contents were measured in the gastrointestinal tract of streptozotocin diabetic rats, 1 month after streptozotocin administration (60 mg/kg), and of age-matched controls with radioimmunoassay. |
| 66 | 1720876 | Substance P and somatostatin contents were statistically increased in the extrafundus of the diabetic stomach, but not in the diabetic fundus. |
| 67 | 1720876 | Changes of substance P and somatostatin contents in the gastrointestinal tract of streptozotocin diabetic rats. |
| 68 | 1720876 | Substance P and somatostatin contents were measured in the gastrointestinal tract of streptozotocin diabetic rats, 1 month after streptozotocin administration (60 mg/kg), and of age-matched controls with radioimmunoassay. |
| 69 | 1720876 | Substance P and somatostatin contents were statistically increased in the extrafundus of the diabetic stomach, but not in the diabetic fundus. |
| 70 | 1720876 | Changes of substance P and somatostatin contents in the gastrointestinal tract of streptozotocin diabetic rats. |
| 71 | 1720876 | Substance P and somatostatin contents were measured in the gastrointestinal tract of streptozotocin diabetic rats, 1 month after streptozotocin administration (60 mg/kg), and of age-matched controls with radioimmunoassay. |
| 72 | 1720876 | Substance P and somatostatin contents were statistically increased in the extrafundus of the diabetic stomach, but not in the diabetic fundus. |
| 73 | 1943736 | Hypothalamic tissue levels of nine regulatory peptides (bombesin, calcitonin gene-related peptide [CGRP], galanin, neuromedin B, neuropeptide Y [NPY], neurotensin, somatostatin, substance P, and vasoactive intestinal peptide [VIP]) were compared in Aston obese diabetic (ob/ob) and lean (+/?) |
| 74 | 2001799 | The pattern of change in the distribution of dopamine-beta-hydroxylase-, substance P-, calcitonin gene-related peptide-, and vasoactive intestinal polypeptide-like immunoreactive nerve fibres that was observed in the ileum from diabetic rats was not evident in the myenteric plexus of distal colon. |
| 75 | 2169207 | For inhibition of binding of 125I-[Tyr4]BN to rat pancreatic tissue, the relative potencies were [D-Phe6]BN-(6-13)ethyl ester (5 nM) greater than Ac-gastrin-releasing peptide (GRP)-(20-26)ethyl ester (17 nM) greater than [D-Phe6,Cpa,14, psi 13-14]BN-(6-14) (40 nM) greater than [Leu14, psi 13-14]BN (0.43 microM) greater than [Tyr4,D-Phe12]BN = [D-Pro4, D-Trp7,9,10]substance P (SP)-4-11 (13 microM) greater than [Leu14, psi 9,10]BN (32 microM) greater than [D-Arg1,D-Trp7,9,Leu11]SP (70 microM). |
| 76 | 2233277 | In contrast, db/db mice of both C57BL/6J and C57BL/KsJ strains exhibited alterations in a total of four peptides in three brain areas: lower concentration of somatostatin-LI in median eminence, higher Met-enkephalin-LI in dorsal vagal complex of the medulla oblongata, higher substance P-LI and lower vasoactive intestinal polypeptide (VIP)-LI in amygdala. |
| 77 | 2262048 | The neuropeptides examined were vasoactive intestinal peptide, neuropeptide Y, substance P. calcitonin gene-related peptide, galanin and somatostatin. |
| 78 | 2262048 | Substance P and calcitonin gene-related peptide which are colocalized in a proportion of the somatostatin neurons were unaffected. |
| 79 | 2262048 | The neuropeptides examined were vasoactive intestinal peptide, neuropeptide Y, substance P. calcitonin gene-related peptide, galanin and somatostatin. |
| 80 | 2262048 | Substance P and calcitonin gene-related peptide which are colocalized in a proportion of the somatostatin neurons were unaffected. |
| 81 | 2412923 | Changes in the somatostatin, substance P and vasoactive intestinal polypeptide content of the gastrointestinal tract following streptozotocin-induced diabetes in the rat. |
| 82 | 2412923 | Rats with streptozotocin-induced diabetes of 10 weeks' duration showed significant changes in the total content of somatostatin, substance P and vasoactive intestinal polypeptide in the stomach and small intestine compared with control animals. |
| 83 | 2412923 | An increase (p less than 0.05) in the concentration and total content of gastric somatostatin and a decrease (p less than 0.05) in the concentration and content of gastric substance P were seen in the streptozotocin-treated rats. |
| 84 | 2412923 | Changes in the somatostatin, substance P and vasoactive intestinal polypeptide content of the gastrointestinal tract following streptozotocin-induced diabetes in the rat. |
| 85 | 2412923 | Rats with streptozotocin-induced diabetes of 10 weeks' duration showed significant changes in the total content of somatostatin, substance P and vasoactive intestinal polypeptide in the stomach and small intestine compared with control animals. |
| 86 | 2412923 | An increase (p less than 0.05) in the concentration and total content of gastric somatostatin and a decrease (p less than 0.05) in the concentration and content of gastric substance P were seen in the streptozotocin-treated rats. |
| 87 | 2412923 | Changes in the somatostatin, substance P and vasoactive intestinal polypeptide content of the gastrointestinal tract following streptozotocin-induced diabetes in the rat. |
| 88 | 2412923 | Rats with streptozotocin-induced diabetes of 10 weeks' duration showed significant changes in the total content of somatostatin, substance P and vasoactive intestinal polypeptide in the stomach and small intestine compared with control animals. |
| 89 | 2412923 | An increase (p less than 0.05) in the concentration and total content of gastric somatostatin and a decrease (p less than 0.05) in the concentration and content of gastric substance P were seen in the streptozotocin-treated rats. |
| 90 | 2417865 | The effect of streptozotocin treatment (65 mg/kg i.v.) on plasma protein extravasation, nociception, and the content of substance P immunoreactivity (SP-IR) and somatostatin immunoreactivity (SOM-IR) was investigated in the rat. |
| 91 | 2428557 | Effect of ganglionic blockade on endogenous circulating pancreatic polypeptide, vasoactive intestinal polypeptide, substance P, neurotensin and noradrenaline in healthy controls and long-term insulin-dependent diabetic patients. |
| 92 | 2428557 | Plasma pancreatic polypeptide (PP), vasoactive intestinal polypeptide (VIP), substance P (SP), neurotensin (NT) and noradrenaline (NA) were measured in eight healthy subjects and 12 long-term insulin-dependent diabetic patients with and without autonomic neuropathy, before and after intravenous infusion of the ganglionic blocking agent trimethaphan camsylate, in order to determine the influence of the autonomic nervous system on the baseline values of the substances. |
| 93 | 2428557 | Effect of ganglionic blockade on endogenous circulating pancreatic polypeptide, vasoactive intestinal polypeptide, substance P, neurotensin and noradrenaline in healthy controls and long-term insulin-dependent diabetic patients. |
| 94 | 2428557 | Plasma pancreatic polypeptide (PP), vasoactive intestinal polypeptide (VIP), substance P (SP), neurotensin (NT) and noradrenaline (NA) were measured in eight healthy subjects and 12 long-term insulin-dependent diabetic patients with and without autonomic neuropathy, before and after intravenous infusion of the ganglionic blocking agent trimethaphan camsylate, in order to determine the influence of the autonomic nervous system on the baseline values of the substances. |
| 95 | 2433176 | Substance P and somatostatin content and transport in vagus and sciatic nerves of the streptozocin-induced diabetic rat. |
| 96 | 2433176 | Substance P (SP) and somatostatin (SS) are two widely distributed neuropeptides that within the vagus and sciatic nerves are localized predominantly in sensory fibers. |
| 97 | 2433176 | Substance P and somatostatin content and transport in vagus and sciatic nerves of the streptozocin-induced diabetic rat. |
| 98 | 2433176 | Substance P (SP) and somatostatin (SS) are two widely distributed neuropeptides that within the vagus and sciatic nerves are localized predominantly in sensory fibers. |
| 99 | 2436255 | Substance P, neurokinin A, vasoactive intestinal polypeptide and gastrin releasing peptide in the intestine and pancreas of spontaneously obese-diabetic mice. |
| 100 | 2436255 | The concentrations and contents of immunoreactive substance P (SP), neurokinin A (NKA), vasoactive intestinal polypeptide (VIP) and gastrin releasing peptide (GRP) were measured in acid-ethanol extracts of intestine (duodenum-jejunum-ileum) and pancreas of C57BL/KsJ diabetes-obese (db/db) mice, Aston obese-hyperglycaemic (ob/ob) mice, and their respective lean controls. |
| 101 | 2436255 | Substance P, neurokinin A, vasoactive intestinal polypeptide and gastrin releasing peptide in the intestine and pancreas of spontaneously obese-diabetic mice. |
| 102 | 2436255 | The concentrations and contents of immunoreactive substance P (SP), neurokinin A (NKA), vasoactive intestinal polypeptide (VIP) and gastrin releasing peptide (GRP) were measured in acid-ethanol extracts of intestine (duodenum-jejunum-ileum) and pancreas of C57BL/KsJ diabetes-obese (db/db) mice, Aston obese-hyperglycaemic (ob/ob) mice, and their respective lean controls. |
| 103 | 2444638 | No change was detected in the total content of noradrenaline in the alveolar lobes or in the levels of vasoactive intestinal polypeptide, neuropeptide Y and substance P in the whole prostates of diabetic rats. |
| 104 | 2454035 | In the present study the ability of two classes of substance P (SP) antagonists to affect SP- and bombesin (Bn)-stimulated amylase release, as well as binding of 125I-Bolton-Hunter (BH)-SP and 125I-[Tyr4]Bn, was studied to determine their mechanism of action and the relationship between inhibition of the action of SP and the action of Bn. |
| 105 | 2454210 | These findings indicate a reduction in the amount of substance P moved by axonal transport in diabetic rats that is related partly to aldose reductase activity and partly to some other insulin-correctable consequence of experimental diabetes. |
| 106 | 2460143 | Because some analogues of substance P can function as receptor antagonists for bombesin as well as substance P, we tested [DPro4,DTrp7,9,10]substance P-4-11 for its ability to modify the interaction of various pancreatic secretagogues with their receptors in dispersed acini from guinea pig pancreas. |
| 107 | 2460143 | [DPro4,DTrp7,9,19]Substance P-4-11 did not stimulate amylase secretion and did not alter the stimulation of amylase secretion caused by secretin, vasoactive intestinal peptide, calcitonin gene-related peptide or carbachol, but did inhibit the stimulation of amylase secretion caused by substance P, bombesin or cholecystokinin. |
| 108 | 2460143 | With substance P, bombesin and cholecystokinin, [DPro4,DTrp7,9,10]substance P-4-11 caused a parallel rightward shift in the dose-response curve for stimulation of amylase secretion with no change in the maximal response. |
| 109 | 2460143 | [DPro4,DTrp7,9,10]Substance P-4-11 inhibited binding of 125I-labeled substance P, 125I-[Tyr4]bombesin and 125I-cholecystokinin octapeptide over the same range of concentrations as that in which it inhibited biologic activity of each of these peptides. |
| 110 | 2460143 | Half-maximal inhibition of binding of 125I-substance P occurred with 4 microM, of 125I-[Tyr4]bombesin with 17 microM and of 125I-cholecystokinin octapeptide with 5 microM. |
| 111 | 2460143 | The present results indicate that [DPro4,DTrp7,9,10]substance P-4-11 is a competitive antagonist at receptors for substance P, for bombesin and for cholecystokinin. |
| 112 | 2460143 | Because some analogues of substance P can function as receptor antagonists for bombesin as well as substance P, we tested [DPro4,DTrp7,9,10]substance P-4-11 for its ability to modify the interaction of various pancreatic secretagogues with their receptors in dispersed acini from guinea pig pancreas. |
| 113 | 2460143 | [DPro4,DTrp7,9,19]Substance P-4-11 did not stimulate amylase secretion and did not alter the stimulation of amylase secretion caused by secretin, vasoactive intestinal peptide, calcitonin gene-related peptide or carbachol, but did inhibit the stimulation of amylase secretion caused by substance P, bombesin or cholecystokinin. |
| 114 | 2460143 | With substance P, bombesin and cholecystokinin, [DPro4,DTrp7,9,10]substance P-4-11 caused a parallel rightward shift in the dose-response curve for stimulation of amylase secretion with no change in the maximal response. |
| 115 | 2460143 | [DPro4,DTrp7,9,10]Substance P-4-11 inhibited binding of 125I-labeled substance P, 125I-[Tyr4]bombesin and 125I-cholecystokinin octapeptide over the same range of concentrations as that in which it inhibited biologic activity of each of these peptides. |
| 116 | 2460143 | Half-maximal inhibition of binding of 125I-substance P occurred with 4 microM, of 125I-[Tyr4]bombesin with 17 microM and of 125I-cholecystokinin octapeptide with 5 microM. |
| 117 | 2460143 | The present results indicate that [DPro4,DTrp7,9,10]substance P-4-11 is a competitive antagonist at receptors for substance P, for bombesin and for cholecystokinin. |
| 118 | 2460143 | Because some analogues of substance P can function as receptor antagonists for bombesin as well as substance P, we tested [DPro4,DTrp7,9,10]substance P-4-11 for its ability to modify the interaction of various pancreatic secretagogues with their receptors in dispersed acini from guinea pig pancreas. |
| 119 | 2460143 | [DPro4,DTrp7,9,19]Substance P-4-11 did not stimulate amylase secretion and did not alter the stimulation of amylase secretion caused by secretin, vasoactive intestinal peptide, calcitonin gene-related peptide or carbachol, but did inhibit the stimulation of amylase secretion caused by substance P, bombesin or cholecystokinin. |
| 120 | 2460143 | With substance P, bombesin and cholecystokinin, [DPro4,DTrp7,9,10]substance P-4-11 caused a parallel rightward shift in the dose-response curve for stimulation of amylase secretion with no change in the maximal response. |
| 121 | 2460143 | [DPro4,DTrp7,9,10]Substance P-4-11 inhibited binding of 125I-labeled substance P, 125I-[Tyr4]bombesin and 125I-cholecystokinin octapeptide over the same range of concentrations as that in which it inhibited biologic activity of each of these peptides. |
| 122 | 2460143 | Half-maximal inhibition of binding of 125I-substance P occurred with 4 microM, of 125I-[Tyr4]bombesin with 17 microM and of 125I-cholecystokinin octapeptide with 5 microM. |
| 123 | 2460143 | The present results indicate that [DPro4,DTrp7,9,10]substance P-4-11 is a competitive antagonist at receptors for substance P, for bombesin and for cholecystokinin. |
| 124 | 2460143 | Because some analogues of substance P can function as receptor antagonists for bombesin as well as substance P, we tested [DPro4,DTrp7,9,10]substance P-4-11 for its ability to modify the interaction of various pancreatic secretagogues with their receptors in dispersed acini from guinea pig pancreas. |
| 125 | 2460143 | [DPro4,DTrp7,9,19]Substance P-4-11 did not stimulate amylase secretion and did not alter the stimulation of amylase secretion caused by secretin, vasoactive intestinal peptide, calcitonin gene-related peptide or carbachol, but did inhibit the stimulation of amylase secretion caused by substance P, bombesin or cholecystokinin. |
| 126 | 2460143 | With substance P, bombesin and cholecystokinin, [DPro4,DTrp7,9,10]substance P-4-11 caused a parallel rightward shift in the dose-response curve for stimulation of amylase secretion with no change in the maximal response. |
| 127 | 2460143 | [DPro4,DTrp7,9,10]Substance P-4-11 inhibited binding of 125I-labeled substance P, 125I-[Tyr4]bombesin and 125I-cholecystokinin octapeptide over the same range of concentrations as that in which it inhibited biologic activity of each of these peptides. |
| 128 | 2460143 | Half-maximal inhibition of binding of 125I-substance P occurred with 4 microM, of 125I-[Tyr4]bombesin with 17 microM and of 125I-cholecystokinin octapeptide with 5 microM. |
| 129 | 2460143 | The present results indicate that [DPro4,DTrp7,9,10]substance P-4-11 is a competitive antagonist at receptors for substance P, for bombesin and for cholecystokinin. |
| 130 | 2460143 | Because some analogues of substance P can function as receptor antagonists for bombesin as well as substance P, we tested [DPro4,DTrp7,9,10]substance P-4-11 for its ability to modify the interaction of various pancreatic secretagogues with their receptors in dispersed acini from guinea pig pancreas. |
| 131 | 2460143 | [DPro4,DTrp7,9,19]Substance P-4-11 did not stimulate amylase secretion and did not alter the stimulation of amylase secretion caused by secretin, vasoactive intestinal peptide, calcitonin gene-related peptide or carbachol, but did inhibit the stimulation of amylase secretion caused by substance P, bombesin or cholecystokinin. |
| 132 | 2460143 | With substance P, bombesin and cholecystokinin, [DPro4,DTrp7,9,10]substance P-4-11 caused a parallel rightward shift in the dose-response curve for stimulation of amylase secretion with no change in the maximal response. |
| 133 | 2460143 | [DPro4,DTrp7,9,10]Substance P-4-11 inhibited binding of 125I-labeled substance P, 125I-[Tyr4]bombesin and 125I-cholecystokinin octapeptide over the same range of concentrations as that in which it inhibited biologic activity of each of these peptides. |
| 134 | 2460143 | Half-maximal inhibition of binding of 125I-substance P occurred with 4 microM, of 125I-[Tyr4]bombesin with 17 microM and of 125I-cholecystokinin octapeptide with 5 microM. |
| 135 | 2460143 | The present results indicate that [DPro4,DTrp7,9,10]substance P-4-11 is a competitive antagonist at receptors for substance P, for bombesin and for cholecystokinin. |
| 136 | 2460143 | Because some analogues of substance P can function as receptor antagonists for bombesin as well as substance P, we tested [DPro4,DTrp7,9,10]substance P-4-11 for its ability to modify the interaction of various pancreatic secretagogues with their receptors in dispersed acini from guinea pig pancreas. |
| 137 | 2460143 | [DPro4,DTrp7,9,19]Substance P-4-11 did not stimulate amylase secretion and did not alter the stimulation of amylase secretion caused by secretin, vasoactive intestinal peptide, calcitonin gene-related peptide or carbachol, but did inhibit the stimulation of amylase secretion caused by substance P, bombesin or cholecystokinin. |
| 138 | 2460143 | With substance P, bombesin and cholecystokinin, [DPro4,DTrp7,9,10]substance P-4-11 caused a parallel rightward shift in the dose-response curve for stimulation of amylase secretion with no change in the maximal response. |
| 139 | 2460143 | [DPro4,DTrp7,9,10]Substance P-4-11 inhibited binding of 125I-labeled substance P, 125I-[Tyr4]bombesin and 125I-cholecystokinin octapeptide over the same range of concentrations as that in which it inhibited biologic activity of each of these peptides. |
| 140 | 2460143 | Half-maximal inhibition of binding of 125I-substance P occurred with 4 microM, of 125I-[Tyr4]bombesin with 17 microM and of 125I-cholecystokinin octapeptide with 5 microM. |
| 141 | 2460143 | The present results indicate that [DPro4,DTrp7,9,10]substance P-4-11 is a competitive antagonist at receptors for substance P, for bombesin and for cholecystokinin. |
| 142 | 2461863 | An increase of vasoactive intestinal polypeptide-, but not neuropeptide Y-, substance P- or catecholamine-containing nerves in the iris of the streptozotocin-induced diabetic rat. |
| 143 | 2461863 | The distribution of adrenergic and vasoactive intestinal polypeptide-, neuropeptide Y- and substance P-immunoreactive nerves was studied histochemically and immunohistochemically in the irides of rats 8 weeks after the induction of diabetes with streptozotocin. |
| 144 | 2461863 | In contrast, no apparent change in the density and/or fluorescence intensity of catecholamine-containing, neuropeptide Y- and substance P-immunoreactive nerve fibres was observed in the irides from diabetic animals when compared with controls. |
| 145 | 2461863 | An increase of vasoactive intestinal polypeptide-, but not neuropeptide Y-, substance P- or catecholamine-containing nerves in the iris of the streptozotocin-induced diabetic rat. |
| 146 | 2461863 | The distribution of adrenergic and vasoactive intestinal polypeptide-, neuropeptide Y- and substance P-immunoreactive nerves was studied histochemically and immunohistochemically in the irides of rats 8 weeks after the induction of diabetes with streptozotocin. |
| 147 | 2461863 | In contrast, no apparent change in the density and/or fluorescence intensity of catecholamine-containing, neuropeptide Y- and substance P-immunoreactive nerve fibres was observed in the irides from diabetic animals when compared with controls. |
| 148 | 2461863 | An increase of vasoactive intestinal polypeptide-, but not neuropeptide Y-, substance P- or catecholamine-containing nerves in the iris of the streptozotocin-induced diabetic rat. |
| 149 | 2461863 | The distribution of adrenergic and vasoactive intestinal polypeptide-, neuropeptide Y- and substance P-immunoreactive nerves was studied histochemically and immunohistochemically in the irides of rats 8 weeks after the induction of diabetes with streptozotocin. |
| 150 | 2461863 | In contrast, no apparent change in the density and/or fluorescence intensity of catecholamine-containing, neuropeptide Y- and substance P-immunoreactive nerve fibres was observed in the irides from diabetic animals when compared with controls. |
| 151 | 2465985 | Chronic pancreatitis and diabetes mellitus: plasma and gastroduodenal mucosal profiles of regulatory peptides (gastrin, motilin, secretin, cholecystokinin, gastric inhibitory polypeptide, somatostatin, VIP, substance P, pancreatic polypeptide, glucagon, enteroglucagon, neurotensin). |
| 152 | 2470551 | In startling contrast, the iris content of substance P-like immunoreactivity was almost trebled in the insulin alone-treated diabetic rats (282% of controls; p less than 0.01), an effect which was prevented completely by sorbinil (127% of controls; not significantly different). |
| 153 | 2473653 | Benzodiazepine analogues L365,260 and L364,718 as gastrin and pancreatic CCK receptor antagonists. |
| 154 | 2473653 | We examined the ability of the recently described 3-(benzoylamino)benzodiazepine analogue L365,260 and the 3-(acylamino)benzodiazepine analogue L364,718 to distinguish gastrin from pancreatic cholecystokinin (CCK) receptors. |
| 155 | 2473653 | Each analogue inhibited CCK-stimulated amylase release, gastrin-17-I-stimulated smooth muscle contraction, binding of 125I-Bolton-Hunter-cholecystokinin octapeptide (125I-BH-CCK-8) to pancreatic CCK receptors, and binding of 125I-gastrin-17-I to gastrin receptors on pancreatic acini. |
| 156 | 2473653 | L365,260 and L364,718 did not inhibit binding of radiolabeled vasoactive intestinal peptide, secretin, bombesin, substance P, or N-methylscopolamine to pancreatic acini. |
| 157 | 2473653 | These results demonstrate that, in contrast to other gastrin-CCK receptor antagonists described, L365,260 is a selective gastrin receptor antagonist having an 80-fold higher affinity for gastrin than pancreatic CCK receptor, whereas L364,718 has a 125-fold higher affinity for pancreatic CCK receptors. |
| 158 | 2473653 | Because of the selectivity of these two antagonists the involvement of CCK and gastrin in various physiological processes can be differentiated even when both receptors occur on the same cell. |
| 159 | 2476475 | Substance P (SP), vasoactive intestinal polypeptide (VIP) and neuropeptide Y (NPY) all stimulated amylase release in untreated rats. |
| 160 | 2476475 | No differences in staining were observed between control and diabetic rats with antisera to tyrosine hydroxylase, substance P. |
| 161 | 2476475 | Substance P (SP), vasoactive intestinal polypeptide (VIP) and neuropeptide Y (NPY) all stimulated amylase release in untreated rats. |
| 162 | 2476475 | No differences in staining were observed between control and diabetic rats with antisera to tyrosine hydroxylase, substance P. |
| 163 | 2478407 | Immunocytochemistry for the general neuronal marker protein gene product 9.5 and four neuropeptides (calcitonin gene-related peptide, substance P, vasoactive intestinal polypeptide and neuropeptide Y) was performed on 20 skin biopsy specimens from 19 diabetic patients, age range 20-75 years, 17 Type 2 (non-insulin-dependent) and 3 Type 1 (insulin-dependent). |
| 164 | 2480400 | Standardised skin biopsies followed by immunohistochemical examination for the presence of terminal nerve fibres reacting for neuropeptides substance P (SP) and calcitonin gene-related peptide (CGRP) were evaluated. |
| 165 | 2480454 | In the hypothalamus and in the striatum of diabetic rats, there are significant higher levels of substance P and met-enkephalin, respectively. |
| 166 | 2480454 | Conversely, in the lumbar cord of diabetic animals, the levels of substance P and met-enkephalin are significantly reduced. |
| 167 | 2480454 | In the hypothalamus and in the striatum of diabetic rats, there are significant higher levels of substance P and met-enkephalin, respectively. |
| 168 | 2480454 | Conversely, in the lumbar cord of diabetic animals, the levels of substance P and met-enkephalin are significantly reduced. |
| 169 | 2579749 | Differential effects of central angiotensin II and substance P on sympathetic nerve activity in conscious rats. |
| 170 | 2579749 | The centrally induced effects of angiotensin II and substance P on the cardiovascular system and on neuronal efferent activity of the splanchnic, renal, and adrenal nerves were investigated in chronically instrumented conscious rats. |
| 171 | 2579749 | It is conceivable that the distinct sympathetic response patterns to central angiotensin II and substance P receptor stimulation form part of a specific cardiovascular adjustment to the individual behavioral reactions, such as drinking, as in the case of angiotensin II, or arousal within the central processing of pain, as in the case of substance P. |
| 172 | 2579749 | Differential effects of central angiotensin II and substance P on sympathetic nerve activity in conscious rats. |
| 173 | 2579749 | The centrally induced effects of angiotensin II and substance P on the cardiovascular system and on neuronal efferent activity of the splanchnic, renal, and adrenal nerves were investigated in chronically instrumented conscious rats. |
| 174 | 2579749 | It is conceivable that the distinct sympathetic response patterns to central angiotensin II and substance P receptor stimulation form part of a specific cardiovascular adjustment to the individual behavioral reactions, such as drinking, as in the case of angiotensin II, or arousal within the central processing of pain, as in the case of substance P. |
| 175 | 2579749 | Differential effects of central angiotensin II and substance P on sympathetic nerve activity in conscious rats. |
| 176 | 2579749 | The centrally induced effects of angiotensin II and substance P on the cardiovascular system and on neuronal efferent activity of the splanchnic, renal, and adrenal nerves were investigated in chronically instrumented conscious rats. |
| 177 | 2579749 | It is conceivable that the distinct sympathetic response patterns to central angiotensin II and substance P receptor stimulation form part of a specific cardiovascular adjustment to the individual behavioral reactions, such as drinking, as in the case of angiotensin II, or arousal within the central processing of pain, as in the case of substance P. |
| 178 | 2593179 | Substance P and met-enkephalin content are remarkably reduced throughout the small intestine, whereas vasoactive intestinal polypeptide levels (VIP) are significantly increased in the duodenum. |
| 179 | 2747219 | Dystrophic axons contained substance P- and gastrin-releasing peptide (gastrin-releasing peptide/bombesin)-like staining but were not labeled by antisera directed against vasoactive intestinal peptide, dynorphin-B, somatostatin, leu- and met-enkephalin and neuropeptide tyrosine. |
| 180 | 2747219 | Substance P and gastrin-releasing peptide/bombesin containing subpopulations of presynaptic elements in prevertebral sympathetic ganglia are thought to participate in local reflex control of bowel motility and lesions preferentially involving these elements may contribute to bowel dysfunction. |
| 181 | 2747219 | Dystrophic axons contained substance P- and gastrin-releasing peptide (gastrin-releasing peptide/bombesin)-like staining but were not labeled by antisera directed against vasoactive intestinal peptide, dynorphin-B, somatostatin, leu- and met-enkephalin and neuropeptide tyrosine. |
| 182 | 2747219 | Substance P and gastrin-releasing peptide/bombesin containing subpopulations of presynaptic elements in prevertebral sympathetic ganglia are thought to participate in local reflex control of bowel motility and lesions preferentially involving these elements may contribute to bowel dysfunction. |
| 183 | 2905198 | Immunohistologic localization of tyrosine hydroxylase (TOH), dopamine-beta-hydroxylase (DBH) and selected neuropeptides (vasoactive intestinal polypeptide, gastrin-releasing peptide (GRP)/bombesin, substance P, Leu-enkephalin, Met-enkephalin, dynorphin B, neuropeptide Y (NPY), somatostatin) was used to investigate the innervation of the small bowel in a rat model of diabetic autonomic neuropathy. |
| 184 | 2908044 | Jejunal tissues from 4- to 5-week diabetic rats were examined for their responses to neurokinin (NK) A, NKB, substance P (SP), bradykinin, neurotensin, bethanechol, isoproterenol and phenylephrine. |
| 185 | 3289997 | Hypothalamic concentrations of the other six peptides examined (bombesin, galanin, neuromedin B, substance P, somatostatin, and vasoactive intestinal peptide) did not differ significantly between STZ-D and control groups at any time. |
| 186 | 3396814 | Mean fasting plasma concentrations of motilin, substance P, and neurotensin from 6 patients did not differ significantly from controls, whereas gastrin and vasoactive intestinal peptide were significantly less than in controls (p less than 0.01). |
| 187 | 3537810 | Using a chemical detection method, a search for previously unknown peptides that possess the C-terminal amide structure in extracts of brain and intestine was carried out and a number of novel neuropeptides and hormonal peptides, designated neuropeptide Y, PHI, peptide YY, galanin and neuropeptide K were isolated. |
| 188 | 6205318 | Changes in the concentration of somatostatin and substance P in the cerebrospinal fluid following injection of alcohol into the pituitary gland. |
| 189 | 6205318 | The concentration of immunoreactive somatostatin and Substance P in the cisternal cerebrospinal fluid (CSF) of patients with pain due to malignant disease has been measured before and after injection of alcohol into the pituitary fossa. |
| 190 | 6205318 | Changes in CSF levels did not correlate with the degree of pain relief obtained, but patients with the greatest increase in somatostatin subsequently developed diabetes insipidus. |
| 191 | 6205318 | Changes in the concentration of somatostatin and substance P in the cerebrospinal fluid following injection of alcohol into the pituitary gland. |
| 192 | 6205318 | The concentration of immunoreactive somatostatin and Substance P in the cisternal cerebrospinal fluid (CSF) of patients with pain due to malignant disease has been measured before and after injection of alcohol into the pituitary fossa. |
| 193 | 6205318 | Changes in CSF levels did not correlate with the degree of pain relief obtained, but patients with the greatest increase in somatostatin subsequently developed diabetes insipidus. |
| 194 | 7472513 | Islet amyloid polypeptide (amylin) is expressed in sensory neurons. |
| 195 | 7472513 | Islet amyloid polypeptide (IAPP) or amylin is a hormone candidate predominantly expressed in insulin cells. |
| 196 | 7472513 | In addition, IAPP-like immunoreactivity occurred in nerve cell bodies storing substance P and pituitary adenylate cyclase-activating polypeptide. |
| 197 | 7513041 | Expression of neuropeptides in experimental diabetes; effects of treatment with nerve growth factor or brain-derived neurotrophic factor. |
| 198 | 7513041 | Treatment of diabetic rats with NGF also prevented the deficits in the levels of CGRP and gamma-PPT mRNA in the lumbar dorsal root ganglia (P < 0.05). |
| 199 | 7513041 | Treatment of other diabetic rats with the related neurotrophin, brain-derived neurotrophic factor (BDNF), had no effect on the levels of substance P and calcitonin gene-related peptide in the sciatic nerve. |
| 200 | 7530343 | Deficits in sciatic nerve neuropeptide content coincide with a reduction in target tissue nerve growth factor messenger RNA in streptozotocin-diabetic rats: effects of insulin treatment. |
| 201 | 7530343 | The levels of substance P and calcitonin gene-related peptide in diabetic sciatic nerve were significantly lowered by approximately 50% and 28%, respectively, compared with aged matched controls and insulin-treated diabetic rats (P < 0.01) for both peptides and both comparisons). |
| 202 | 7530343 | Measurements of nerve growth factor messenger RNA levels in sensory neuron target tissues, namely foot-skin and soleus muscle, revealed deficits of approximately 50% in diabetic rats, with insulin treatment reversing the decrease in foot-skin but not in soleus muscle. |
| 203 | 7530767 | Nerve growth factor (NGF) restores depletions of calcitonin gene-related peptide and substance P in sensory neurons from diabetic mice in vitro. |
| 204 | 7530767 | The ratios of neurons immunoreactive to CGRP and substance P (SP) in the NGF-free medium were also lower in the genetic diabetic mice (23.6% and 21.8%) than those in the normal ones (40.7% and 34.2%). |
| 205 | 7530767 | These results show that NGF can be effective for the diabetes-induced depletion of CGRP and SP in sensory neurons, and suggest its possible role in the prevention and improvement of diabetic sensory neuropathy. |
| 206 | 7530767 | Nerve growth factor (NGF) restores depletions of calcitonin gene-related peptide and substance P in sensory neurons from diabetic mice in vitro. |
| 207 | 7530767 | The ratios of neurons immunoreactive to CGRP and substance P (SP) in the NGF-free medium were also lower in the genetic diabetic mice (23.6% and 21.8%) than those in the normal ones (40.7% and 34.2%). |
| 208 | 7530767 | These results show that NGF can be effective for the diabetes-induced depletion of CGRP and SP in sensory neurons, and suggest its possible role in the prevention and improvement of diabetic sensory neuropathy. |
| 209 | 7534145 | This study examined the expression of the sensory neuropeptides, calcitonin gene-related peptide (CGRP) and substance P (SP), in the lumbar 4 and 5 dorsal root ganglion (DRG) and spinal cord of spontaneously diabetic BB rats and non-diabetic controls using quantitative immunohistochemical analysis. |
| 210 | 7536686 | In our study we have used morphological and radio-immunological methods for the investigation of calcitonin gene-related peptide (CGRP) and substance P in cervical dorsal root ganglia (DRGs) in mice after administration of taxol or cisplatin and in spontaneously diabetic animals (db/db mice). |
| 211 | 7536686 | Application of 10 mg/kg NGF caused a significant elevation in peptide-immunoreactivity in control animals and in taxol-treated mice, i.e., statistically significant increase in peptide concentrations and in the number of substance P- and CGRP-immunoreactive DRG-neurons, suggesting a recruitment of additional peptide cells. |
| 212 | 7536686 | In diabetic animals a restoration in CGRP-content was observed under NGF-treatment; however, in this model the quantitative parameters did not demonstrate further elevation above control levels. |
| 213 | 7536686 | In our study we have used morphological and radio-immunological methods for the investigation of calcitonin gene-related peptide (CGRP) and substance P in cervical dorsal root ganglia (DRGs) in mice after administration of taxol or cisplatin and in spontaneously diabetic animals (db/db mice). |
| 214 | 7536686 | Application of 10 mg/kg NGF caused a significant elevation in peptide-immunoreactivity in control animals and in taxol-treated mice, i.e., statistically significant increase in peptide concentrations and in the number of substance P- and CGRP-immunoreactive DRG-neurons, suggesting a recruitment of additional peptide cells. |
| 215 | 7536686 | In diabetic animals a restoration in CGRP-content was observed under NGF-treatment; however, in this model the quantitative parameters did not demonstrate further elevation above control levels. |
| 216 | 7538256 | There were no differences between the groups with respect to density and distribution of nerve fibers displaying immunoreactivity to the pan-neuronal marker PGP 9.5 and sensory and parasympathetic neuropeptides (substance P, calcitonin gene-related peptide and vasoactive intestinal peptide). |
| 217 | 7562555 | Tiapride dose-dependently attenuated the biphasic nociceptive responses induced by s.c. injection of formalin to the hindpaw of mice, and its activity on the first (ED50 = 110 mg/kg p.o.) and the second (ED50 = 32.0 mg/kg p.o.) phases paralleled that on the nociceptive response to intrathecal injection of substance P (ED50 = 190 mg/kg p.o.) and somatostatin (ED50 = 56.0 mg/kg p.o.), respectively. |
| 218 | 7562555 | The effects of tiapride (100 mg/kg p.o.) on both phases of the formalin test in normal mice were abolished by pretreatment with p-chlorophenylalanine (800 x 2 mg/kg p.o.), a 5-hydroxytryptamine (5-HT) depletor, or pindolol (1 mg/kg i.p.), a 5-HT1 antagonist, but were scarcely affected by 3-tropanyl-indole-3-carboxylate, a 5-HT3 antagonist. |
| 219 | 7562561 | Recently it has been established that both a gastrin-releasing peptide (GRP) receptor and a neuromedin B (NMB) receptor mediate the actions of bombesin-related peptides in mammals. |
| 220 | 7562561 | Five different classes of peptides that function as GRP receptor antagonists have been identified; however, it is unknown whether similar strategies will yield antagonists for the closely related NMB receptor. |
| 221 | 7562561 | In the present study we have used either native cells possessing only one bombesin (Bn) receptor subtype or cells stably transfected with one subtype to determine whether using the strategies that were used successfully for GRP receptors would allow NMB receptor antagonists to be identified. |
| 222 | 7562561 | [DPhe12]Bn analogs; des Met14 amides, esters and alkylamides; psi 13-14 Bn pseudopeptides; and D-amino acid-substituted analogs of substance P (SP) or SP(4-11) were all synthesized and each functioned as a GRP receptor antagonist. |
| 223 | 7562561 | All of these antagonists had low affinity for the NMB receptor. |
| 224 | 7562561 | Application of similar strategies to NMB by formation of [DPhe8]NMB, [psi 9-10]NMB pseudopeptides, des-Met10 NMB amides, alkylamide or esters did not result in any potent NMB receptor antagonists. |
| 225 | 7562561 | D-Amino acid SP and SP(4-11) analogs were weakly selective NMB receptor antagonists. |
| 226 | 7562561 | No COOH-terminal fragments of NMB or GRP functioned as a GRP or NMB receptor antagonist. |
| 227 | 7562561 | These results demonstrate that none of the known strategies used to prepare peptide GRP receptor antagonists are successful at the NMB receptor, suggesting that a different strategy will be needed for this peptide, such as the formation of somatostatin octapeptide or D-amino acid-substituted substance P analogs. |
| 228 | 7562561 | These results suggest that even though there is a close homology between GRP and NMB and their receptors, their structure-function relations are markedly different. |
| 229 | 7562561 | Recently it has been established that both a gastrin-releasing peptide (GRP) receptor and a neuromedin B (NMB) receptor mediate the actions of bombesin-related peptides in mammals. |
| 230 | 7562561 | Five different classes of peptides that function as GRP receptor antagonists have been identified; however, it is unknown whether similar strategies will yield antagonists for the closely related NMB receptor. |
| 231 | 7562561 | In the present study we have used either native cells possessing only one bombesin (Bn) receptor subtype or cells stably transfected with one subtype to determine whether using the strategies that were used successfully for GRP receptors would allow NMB receptor antagonists to be identified. |
| 232 | 7562561 | [DPhe12]Bn analogs; des Met14 amides, esters and alkylamides; psi 13-14 Bn pseudopeptides; and D-amino acid-substituted analogs of substance P (SP) or SP(4-11) were all synthesized and each functioned as a GRP receptor antagonist. |
| 233 | 7562561 | All of these antagonists had low affinity for the NMB receptor. |
| 234 | 7562561 | Application of similar strategies to NMB by formation of [DPhe8]NMB, [psi 9-10]NMB pseudopeptides, des-Met10 NMB amides, alkylamide or esters did not result in any potent NMB receptor antagonists. |
| 235 | 7562561 | D-Amino acid SP and SP(4-11) analogs were weakly selective NMB receptor antagonists. |
| 236 | 7562561 | No COOH-terminal fragments of NMB or GRP functioned as a GRP or NMB receptor antagonist. |
| 237 | 7562561 | These results demonstrate that none of the known strategies used to prepare peptide GRP receptor antagonists are successful at the NMB receptor, suggesting that a different strategy will be needed for this peptide, such as the formation of somatostatin octapeptide or D-amino acid-substituted substance P analogs. |
| 238 | 7562561 | These results suggest that even though there is a close homology between GRP and NMB and their receptors, their structure-function relations are markedly different. |
| 239 | 7613616 | These deficits correlated with reductions in substance P and calcitonin gene-related peptide--both products of NGF-influenced genes in primary afferents. |
| 240 | 7613616 | These manifestations of deficient neurotrophic support were corrected by intensive insulin treatment and surmounted by administration of exogenous human recombinant NGF in a dose-related manner. |
| 241 | 7628782 | We already reported about the allelic distribution, changes of plaque formation and body weight, biochemical nature, toxic activity, vascular permeability factor and bradykinin inactivating factor of the plaque, histological and immunological studies, the pH in the periodontal pocket, amount of saliva, IgA in the saliva, salivary kallikrein, the relationship between sialic acid in the saliva and the serum, leukocyte functions (chemotaxis and superoxide anion) in ODUS/Odu, histamine, mast cell, free radicals, superoxide dismutase activities in gingiva and gingival nerve fibers with substance P or calcitonin gene-related peptide, and effect of diabetes. |
| 242 | 7678435 | Nociceptive responses to intrathecally administered substance P and somatostatin in diabetic mice. |
| 243 | 7678435 | The nociceptive behavioral responses to i.t. injection of somatostatin (SST) but nor substance P (SP) were attenuated in diabetic mice compared with that in non-diabetic mice. |
| 244 | 7678435 | Nociceptive responses to intrathecally administered substance P and somatostatin in diabetic mice. |
| 245 | 7678435 | The nociceptive behavioral responses to i.t. injection of somatostatin (SST) but nor substance P (SP) were attenuated in diabetic mice compared with that in non-diabetic mice. |
| 246 | 7682680 | These results suggest that a negative control system, which is mediated by delta-opioid receptors and links substance P with somatostatin-mediated nociceptive transmission, may inhibit the formalin-induced second-phase of the nociceptive response in diabetic mice. |
| 247 | 7683174 | The effects of either substance P (SP) or a metabolically stable SP analogue, [pGlu5,Me-Phe8,Sar9]SP(5-11), alone or in combination with calcitonin gene-related peptide (CGRP) on blood pressure (BP) and extravasation of serum albumin were examined in normal and diabetic rats. |
| 248 | 7686682 | We also investigated the effects of mexiletine on intrathecally-administered substance P- and somatostatin-induced nociceptive responses in both non-diabetic and diabetic mice. |
| 249 | 7689105 | This study investigates the ability of two chimeric galanin analogs, [# 1-galantide = (M-15) = [galanin (1-13)-substance P(5-11)] and #2-M-35[galanin(1-13)bradykinin (2-9)], which were recently reported to function as galanin-receptor antagonists in the CNS, to interact with galanin receptors on rat jejunal muscle strips or dispersed smooth muscle cells from guinea pig stomach. |
| 250 | 7689105 | In dispersed smooth muscle cells, galanin, as well as each chimeric analog, caused muscle relaxation, whereas substance P and bradykinin both caused muscle contraction. |
| 251 | 7689105 | This study investigates the ability of two chimeric galanin analogs, [# 1-galantide = (M-15) = [galanin (1-13)-substance P(5-11)] and #2-M-35[galanin(1-13)bradykinin (2-9)], which were recently reported to function as galanin-receptor antagonists in the CNS, to interact with galanin receptors on rat jejunal muscle strips or dispersed smooth muscle cells from guinea pig stomach. |
| 252 | 7689105 | In dispersed smooth muscle cells, galanin, as well as each chimeric analog, caused muscle relaxation, whereas substance P and bradykinin both caused muscle contraction. |
| 253 | 7689996 | Functional changes in the urinary bladder obtained from streptozotocin-induced diabetic rats were investigated by determining the responsiveness of bladder strips to capsaicin or substance P (SP). 2. |
| 254 | 7694856 | The effect of inhibiting nitric oxide synthase (N omega-nitro-L-arginine) on plasma extravasation induced by intravenously administered substance P, [pGlu5,Me-Phe8,Sar9]substance P-(5-11) or prostaglandin E2 was examined. |
| 255 | 7694865 | These results suggest that (i) substance P is involved in the diabetes-induced chronic hyperalgesia, and (ii) NK1 receptor antagonists merit to be studied more extensively in relation with this pathological condition. |
| 256 | 7769988 | Changes in nerve growth factor and preprotachykinin messenger RNA levels in the iris and trigeminal ganglion in diabetic rats; effects of treatment with insulin or nerve growth factor. |
| 257 | 7769988 | This study was designed to explore effects of experimental diabetes mellitus on expression of substance P in the trigeminal ganglion and of nerve growth factor (NGF) in the iris. |
| 258 | 7769988 | Rats with streptozotocin-diabetes showed an increase in NGF mRNA in the iris (P < 0.01) which was corrected by insulin treatment. |
| 259 | 7769988 | There was also an increase in the levels of mRNA for the substance P precursor, preprotachykinin (PPT), in the trigeminal ganglion of these animals, despite there being no change in GAP-43 mRNA. |
| 260 | 7769988 | There was a dose-dependent increase in both gamma-PPT and GAP-43 mRNA in the trigeminal ganglia of NGF-treated diabetic rats. |
| 261 | 7769988 | The findings indicate that increased NGF may be responsible for raised substance P levels in the iris. |
| 262 | 7769988 | Changes in nerve growth factor and preprotachykinin messenger RNA levels in the iris and trigeminal ganglion in diabetic rats; effects of treatment with insulin or nerve growth factor. |
| 263 | 7769988 | This study was designed to explore effects of experimental diabetes mellitus on expression of substance P in the trigeminal ganglion and of nerve growth factor (NGF) in the iris. |
| 264 | 7769988 | Rats with streptozotocin-diabetes showed an increase in NGF mRNA in the iris (P < 0.01) which was corrected by insulin treatment. |
| 265 | 7769988 | There was also an increase in the levels of mRNA for the substance P precursor, preprotachykinin (PPT), in the trigeminal ganglion of these animals, despite there being no change in GAP-43 mRNA. |
| 266 | 7769988 | There was a dose-dependent increase in both gamma-PPT and GAP-43 mRNA in the trigeminal ganglia of NGF-treated diabetic rats. |
| 267 | 7769988 | The findings indicate that increased NGF may be responsible for raised substance P levels in the iris. |
| 268 | 7769988 | Changes in nerve growth factor and preprotachykinin messenger RNA levels in the iris and trigeminal ganglion in diabetic rats; effects of treatment with insulin or nerve growth factor. |
| 269 | 7769988 | This study was designed to explore effects of experimental diabetes mellitus on expression of substance P in the trigeminal ganglion and of nerve growth factor (NGF) in the iris. |
| 270 | 7769988 | Rats with streptozotocin-diabetes showed an increase in NGF mRNA in the iris (P < 0.01) which was corrected by insulin treatment. |
| 271 | 7769988 | There was also an increase in the levels of mRNA for the substance P precursor, preprotachykinin (PPT), in the trigeminal ganglion of these animals, despite there being no change in GAP-43 mRNA. |
| 272 | 7769988 | There was a dose-dependent increase in both gamma-PPT and GAP-43 mRNA in the trigeminal ganglia of NGF-treated diabetic rats. |
| 273 | 7769988 | The findings indicate that increased NGF may be responsible for raised substance P levels in the iris. |
| 274 | 8024263 | Neuropeptide expression is plastic; during development, neurons that switch from a noradrenergic to a cholinergic phenotype increase expression of vasoactive intestinal polypeptide, somatostatin, and substance P. |
| 275 | 8024263 | Preganglionic inputs increase neuropeptide Y and inhibit substance P expression. |
| 276 | 8024263 | Neuropeptide expression is plastic; during development, neurons that switch from a noradrenergic to a cholinergic phenotype increase expression of vasoactive intestinal polypeptide, somatostatin, and substance P. |
| 277 | 8024263 | Preganglionic inputs increase neuropeptide Y and inhibit substance P expression. |
| 278 | 8549856 | However, there was no change in the density of neuropeptide Y- and dopamine beta-hydroxylase-immunoreactive nerve fibers, although the fluorescence intensity of neuropeptide Y-immunoreactive nerve fibers was reduced in diabetic rat vessels. |
| 279 | 8549856 | Immunoassays showed that the levels of substance P- and calcitonin gene-related peptide were increased > 10-fold in the diabetic mesenteric vein, while levels of neuropeptide Y and vasoactive intestinal polypeptide were unchanged. |
| 280 | 8614263 | Effects of streptozotocin-induced diabetes and insulin treatment on substance P of the rat arterial wall. |
| 281 | 8640566 | We describe an early length-dependent dysfunction of sensory small-diameter fibers, prior to dysfunction of sympathetic fibers, with depletion of skin NGF and the sensory neuropeptide substance P. |
| 282 | 8640566 | We describe a significant correlation between NGF depletion and decreased skin axon-reflex vasodilation, mediated by small sensory fibers partly via substance P release. |
| 283 | 8640566 | We describe an early length-dependent dysfunction of sensory small-diameter fibers, prior to dysfunction of sympathetic fibers, with depletion of skin NGF and the sensory neuropeptide substance P. |
| 284 | 8640566 | We describe a significant correlation between NGF depletion and decreased skin axon-reflex vasodilation, mediated by small sensory fibers partly via substance P release. |
| 285 | 8672532 | Binding of 125I-BH-SP was saturable, reversible, time- and temperature-dependent and was inhibited by several SP-related peptides with relative potencies of SP = physalaemin (IC50:0.19 nM) > SP methyl ester (SP-ME) (IC50:3.3 nM) > eledoisin (IC50:6.1 nM) > neurokinin A (NKA) (IC50: 65 nM) > neurokinin B (NKB) (IC50:80 nM). |
| 286 | 8672532 | Phospholipase C activating agents (carbachol, CCK-8), adenylate cyclase activating agents (secretin, VIP), TPA and the calcium ionophore, A23187, all inhibited the binding of 125I-BH-SP and it was due to inhibition of ligand internalization with no change in surface bound parameters. |
| 287 | 8672532 | In conclusion, the present study demonstrates that chief cells possess a NK1 subtype of tachykinin receptor, occupation of the low affinity sites of this receptor cause calcium mobilization and pepsinogen secretion, and that binding to this receptor is regulated by agents that activate phospholipase C, adenylate cyclase, protein kinase C and calcium mobilization. |
| 288 | 8730784 | In diabetics, there was an early length-dependent dysfunction of small-diameter sensory fibres, with depletion of skin NGF and the sensory neuropeptide substance P. |
| 289 | 8730784 | The NGF depletion correlated significantly with decreased skin axon-reflex vasodilatation, which is mediated by small sensory fibres at least partly via substance P release. |
| 290 | 8730784 | In diabetics, there was an early length-dependent dysfunction of small-diameter sensory fibres, with depletion of skin NGF and the sensory neuropeptide substance P. |
| 291 | 8730784 | The NGF depletion correlated significantly with decreased skin axon-reflex vasodilatation, which is mediated by small sensory fibres at least partly via substance P release. |
| 292 | 8730785 | In rodent models of diabetes there are expression deficits in nerve growth factor (NGF) and in its high-affinity receptor, trkA, leading to decreased retrograde axonal transport of NGF and decreased support of NGF-dependent sensory neurons, with reduced expression of their neuropeptides, substance P and calcitonin gene-related peptide (CGRP). |
| 293 | 8730785 | Treatment of diabetic rats with intensive insulin normalized these deficits and treatment with exogenous NGF caused dose-related increases, giving levels of NGF and neuropeptides which were greater than those of controls. |
| 294 | 8738148 | Regenerating sensory neurones of diabetic rats express reduced levels of mRNA for GAP-43, gamma-preprotachykinin and the nerve growth factor receptors, trkA and p75NGFR. |
| 295 | 8738148 | This study was designed to measure expression of messenger RNA (mRNA) coding for NGF and its receptors, trkA and p75NGFR, during nerve regeneration and degeneration in rats with streptozotocin-induced diabetes; mRNA coding for preprotachykinin A (the substance P precursor), whose expression is stimulated by NGF, and mRNA for growth-associated protein-43 (GAP-43) were also measured in blots from L4 + L5 (pooled unilaterally) dorsal root ganglia. |
| 296 | 8738309 | Enteric neuropeptides in streptozotocin-diabetic rats; effects of insulin and aldose reductase inhibition. |
| 297 | 8738309 | The aim of the present study was to determine whether diabetes-induced changes in the distribution of enteric neuropeptides, could be prevented in 12-week streptozotocin-diabetic rats, by rigorous control of glycaemia, using daily adminstration of insulin, or an aldose reductase inhibitor (ponalrestat). |
| 298 | 8738309 | The pattern of distribution of nerve fibres and cell bodies, containing immunoreactive vasoactive intestinal polypeptide (VIP), galanin (GAL), calcitonin gene-related peptide (CGRP) and substance P was examined in the myenteric plexus of ileum from control, untreated diabetic, insulin-treated diabetic and aldose reductase inhibitor-treated diabetic rats. |
| 299 | 8738309 | The increase in VIP- and GAL-like immunoreactivity, seen in the myenteric plexus of untreated diabetic rat ileum, was not present in the myenteric plexus of ileum from insulin- and aldose reductase inhibitor-treated diabetic rats. |
| 300 | 8738309 | This was prevented by insulin treatment, but aldose reductase inhibitor treatment had no effect. |
| 301 | 8738309 | Generally, the similarity of effect of ponalrestat and insulin on VIP and galanin expression in this study supports a primary effect of insulin via glycaemic control. |
| 302 | 8738309 | The dissimilarity of the effect of the two treatments on CGRP expression may imply a neurotrophic effect of insulin, although there are certainly consequences of hyperglycaemia other than exaggerated flux through the polyol pathway. |
| 303 | 8739322 | Pituitary contents of beta-endorphin, dynorphin, substance P, cholecystokinin and somatostatin in rats with streptozotocin-induced diabetes. |
| 304 | 8739322 | Substance P, dynorphin and beta-endorphin in both pituitary lobes and cholecystokinin and somatostatin in the neurointermediate lobe (NIL) were measured 4 weeks after streptozotocin treatment in adult male rats. |
| 305 | 8739322 | There were significant decreases of substance P levels in both the anterior lobe (AL) and NIL, and of cholecystokinin, dynorphin and beta-endorphin in the NIL, whereas the dynorphin content in the AL increased, when values were expressed on a per-lobe basis. |
| 306 | 8739322 | Pituitary contents of beta-endorphin, dynorphin, substance P, cholecystokinin and somatostatin in rats with streptozotocin-induced diabetes. |
| 307 | 8739322 | Substance P, dynorphin and beta-endorphin in both pituitary lobes and cholecystokinin and somatostatin in the neurointermediate lobe (NIL) were measured 4 weeks after streptozotocin treatment in adult male rats. |
| 308 | 8739322 | There were significant decreases of substance P levels in both the anterior lobe (AL) and NIL, and of cholecystokinin, dynorphin and beta-endorphin in the NIL, whereas the dynorphin content in the AL increased, when values were expressed on a per-lobe basis. |
| 309 | 8739322 | Pituitary contents of beta-endorphin, dynorphin, substance P, cholecystokinin and somatostatin in rats with streptozotocin-induced diabetes. |
| 310 | 8739322 | Substance P, dynorphin and beta-endorphin in both pituitary lobes and cholecystokinin and somatostatin in the neurointermediate lobe (NIL) were measured 4 weeks after streptozotocin treatment in adult male rats. |
| 311 | 8739322 | There were significant decreases of substance P levels in both the anterior lobe (AL) and NIL, and of cholecystokinin, dynorphin and beta-endorphin in the NIL, whereas the dynorphin content in the AL increased, when values were expressed on a per-lobe basis. |
| 312 | 8740660 | The effect of acrylamide intoxication (a widely used model for autonomic neuropathy) on the fluorescence intensity and density of catecholamine- and peptide-containing nerve fibres and tissue content of noradrenaline and the peptides vasoactive intestinal polypeptide, calcitonin gene-related peptide, substance P and neuropeptide Y in the enteric nerves of rat ileum was examined. |
| 313 | 8830848 | Preprotachykinin (PPT) mRNA encoding the peptide substance P (SP), has been localized in the anterior pituitary. |
| 314 | 8899822 | Somatostatin (SOM), calcitenin gene-related peptide (CGRP), and substance P (SP) are neuropeptides that modulate pain responses transmitted by primary sensory afferents, the cell bodies of which are located in the dorsal root ganglion (DRG). |
| 315 | 8899822 | These data suggest that CGRP and SOM synthesis in primary sensory neurons is reduced in STZ-induced diabetic rats. |
| 316 | 9010501 | The salivary glands of non-obese diabetic (NOD) mice and BALB/c controls were evaluated for the stimulatory effects of the following neuropeptides; substance P (SP), vasoactive intestinal polypeptide (VIP), and neuropeptide Y (NPY). |
| 317 | 9013783 | Effect of streptozotocin-diabetes on knee joint inflammation-induced changes in substance P and nerve growth factor in the rat. |
| 318 | 9013783 | After 24 weeks of streptozotocin-diabetes, there was a non-significant reduction in gamma-preprotachykinin mRNA expression whilst substance P levels in dorsal root ganglia, sciatic nerve and synovium and nerve growth factor levels in the sciatic nerve were significantly decreased. |
| 319 | 9013783 | Substance P levels were unaltered compared to non-arthritic diabetic rats whilst nerve growth factor levels were significantly increased in synovium and sciatic nerve suggesting an uncoupling of substance P from nerve growth factor control in the inflammatory response in diabetic rats. |
| 320 | 9013783 | Deficits in gamma-preprotachykinin mRNA expression and substance P and the altered levels of nerve growth factor indicate sensory neuronal dysfunction may play a major role in this abnormal response. |
| 321 | 9013783 | Effect of streptozotocin-diabetes on knee joint inflammation-induced changes in substance P and nerve growth factor in the rat. |
| 322 | 9013783 | After 24 weeks of streptozotocin-diabetes, there was a non-significant reduction in gamma-preprotachykinin mRNA expression whilst substance P levels in dorsal root ganglia, sciatic nerve and synovium and nerve growth factor levels in the sciatic nerve were significantly decreased. |
| 323 | 9013783 | Substance P levels were unaltered compared to non-arthritic diabetic rats whilst nerve growth factor levels were significantly increased in synovium and sciatic nerve suggesting an uncoupling of substance P from nerve growth factor control in the inflammatory response in diabetic rats. |
| 324 | 9013783 | Deficits in gamma-preprotachykinin mRNA expression and substance P and the altered levels of nerve growth factor indicate sensory neuronal dysfunction may play a major role in this abnormal response. |
| 325 | 9013783 | Effect of streptozotocin-diabetes on knee joint inflammation-induced changes in substance P and nerve growth factor in the rat. |
| 326 | 9013783 | After 24 weeks of streptozotocin-diabetes, there was a non-significant reduction in gamma-preprotachykinin mRNA expression whilst substance P levels in dorsal root ganglia, sciatic nerve and synovium and nerve growth factor levels in the sciatic nerve were significantly decreased. |
| 327 | 9013783 | Substance P levels were unaltered compared to non-arthritic diabetic rats whilst nerve growth factor levels were significantly increased in synovium and sciatic nerve suggesting an uncoupling of substance P from nerve growth factor control in the inflammatory response in diabetic rats. |
| 328 | 9013783 | Deficits in gamma-preprotachykinin mRNA expression and substance P and the altered levels of nerve growth factor indicate sensory neuronal dysfunction may play a major role in this abnormal response. |
| 329 | 9013783 | Effect of streptozotocin-diabetes on knee joint inflammation-induced changes in substance P and nerve growth factor in the rat. |
| 330 | 9013783 | After 24 weeks of streptozotocin-diabetes, there was a non-significant reduction in gamma-preprotachykinin mRNA expression whilst substance P levels in dorsal root ganglia, sciatic nerve and synovium and nerve growth factor levels in the sciatic nerve were significantly decreased. |
| 331 | 9013783 | Substance P levels were unaltered compared to non-arthritic diabetic rats whilst nerve growth factor levels were significantly increased in synovium and sciatic nerve suggesting an uncoupling of substance P from nerve growth factor control in the inflammatory response in diabetic rats. |
| 332 | 9013783 | Deficits in gamma-preprotachykinin mRNA expression and substance P and the altered levels of nerve growth factor indicate sensory neuronal dysfunction may play a major role in this abnormal response. |
| 333 | 9114037 | NK1- and NK2-specific clones recognize two groups of HLA-C allotypes that are distinguished by a dimorphism at residue 80 in the alpha1 helix (alphaLys-80 and alphaAsn-80, respectively). |
| 334 | 9148247 | This study compared the effects of treatment of diabetic rats with either alpha-lipoic acid (100 mg/kg/day i.p. 5 days/week) or with recombinant human nerve growth factor (rhNGF; 0.2 mg/kg s.c. 3 days/week) on NGF-like immunoreactivity (NGFLI) and neuropeptide Y-like immunoreactivity (NPYLI) levels in the sciatic nerve and on the release of substance P-like immunoreactivity (SPLI) from the spinal cord in response to electrical stimulation of the dorsal roots in vitro. |
| 335 | 9225823 | Substance P (SP), vasoactive intestinal polypeptide (VIP), and somatostatin content in rectal mucosa were determined by radioimmunoassay (RIA) in 38 diabetic patients (12 with normal bowel function, 13 with diabetic diarrhea, and 13 with constipation) and in 10 nondiabetic controls with normal bowel function. |
| 336 | 9272460 | In addition, dilatation of arterioles in response to histamine and substance P in nondiabetic hamsters was abolished by application of an enzymatic inhibitor of nitric oxide synthase (L-NMMA). |
| 337 | 9285498 | In rodent models of diabetes, there are expression deficits in nerve growth factor (NGF) and in mRNA for its high-affinity receptor, trkA, leading to decreased retrograde axonal transport of NGF and decreased support of NGF-dependent sensory neurons, with reduced expression of their neuropeptides, substance P and calcitonin gene-related peptide (CGRP). |
| 338 | 9285498 | Treatment of diabetic rats with intensive insulin normalized these deficits, and treatment with exogenous NGF caused dose-related increases, giving levels of NGF and neuropeptides that were greater than those of controls. |
| 339 | 9285498 | In regenerating nerves after experimental crush injury, expression of NGF in the nerve trunk is increased in diabetes to a greater extent than in controls, but this is offset by a greater reduction in the neuronal expression of trkA in dorsal root ganglia of diabetic rats. |
| 340 | 9566647 | The tumour was diagnosed histopathologically as a moderately differentiated adenocarcinoma with focal neuroendocrine cell differentiation and dispersed cells reacting with antisera against neurone-specific enolase, S-100 protein, neuropeptide Y, follicle-stimulating hormone, substance P, vasoactive polypeptide (VIP), adrenocorticotropic hormone and pancreatic polypeptide (PP) as well as to one of three tested antisera raised against antidiuretic hormone (ADH). |
| 341 | 9593699 | Ability of various bombesin receptor agonists and antagonists to alter intracellular signaling of the human orphan receptor BRS-3. |
| 342 | 9593699 | Bombesin (Bn) receptor subtype 3 (BRS-3) is an orphan receptor that is a predicted member of the heptahelical G-protein receptor family and so named because it shares a 50% amino acid homology with receptors for the mammalian bombesin-like peptides neuromedin B (NMB) and gastrin-releasing peptide. |
| 343 | 9593699 | [D-Phe6,beta-Ala11,Phe13,Nle14]Bn-(6-14) stimulated a 2-3-fold increase in [Ca2+]i, a 3-fold increase in tyrosine phosphorylation of p125(FAK) with an EC50 of 0.2-0.7 nM, but failed to either stimulate increases in cyclic AMP or inhibit forskolin-stimulated increases. |
| 344 | 9593699 | No high affinity Bn receptor antagonists had high affinity for the hBRS-3 receptor, although two low affinity antagonists for gastrin-releasing peptide and NMB receptors, [D-Arg1,D-Trp7,9, Leu11]substance P and [D-Pro4,D-Trp7,9,10]substance P-(4-11), inhibited hBRS-3 receptor activation. |
| 345 | 9593699 | The NMB receptor-specific antagonist D-Nal,Cys,Tyr,D-Trp,Lys,Val, Cys,Nal-NH2 inhibited hBRS-3 receptor activation in a competitive fashion (Ki = 0.5 microM). |
| 346 | 9593699 | Stimulation of p125(FAK) tyrosine phosphorylation by hBRS-3 activation was not inhibited by the protein kinase C inhibitor, GF109203X, or thapsigargin, alone or in combination. |
| 347 | 9593699 | These results show that hBRS-3 receptor activation increases phospholipase C activity, which causes generation of inositol phosphates and changes in [Ca2+]i and is also coupled to tyrosine kinase activation, but is not coupled to adenylate cyclase activation or inhibition. hBRS-3 receptor activation results in tyrosine phosphorylation of p125(FAK), and it is not dependent on activation of either limb of the phospholipase C cascade. |
| 348 | 9618426 | The intracerebroventricular (10-100 microg/animal) but not systemic administration of PD 156982 (1-100 mg/kg, s.c.) blocked the [Sar9, Met(O2)11] substance P-induced gerbil foot tapping response. |
| 349 | 9686927 | Untreated streptozotocin-diabetic (7 weeks duration) rats showed reductions (all p < 0.01; percentages in brackets) in motor and sensory nerve conduction velocity (MNCV; 14%, SNCV; 17%) and in sciatic nerve contents of nerve growth factor (NGF; 57%), substance P (SP; 53%) and neuropeptide Y (NPY; 39%). |
| 350 | 9686927 | Treatment with a gamma-linolenic acid-alpha-lipoic acid conjugate (GLA-LA; 35 mg x day(-1) x rat(-1)) attenuated (p < 0.05) these reductions to MNCV (8%), SNCV (5%), NGF (19%), SP (23%), NPY (20%), such that the values in GLA-LA-treated diabetic rats did not differ significantly from those of control non-diabetic animals. |
| 351 | 9696468 | The non-peptide antagonist for the substance P, neurokinin, (NK1) receptor, RP 67580 (3-9 mg/kg i.p.) was not effective in reversing the mechanical hyperalgesia associated with 4 week-diabetes. |
| 352 | 9743564 | These changes occurred in the entire myelinated population of sensory nerves and were not restricted to nociceptive nerve fibers. (2) The NGF effect on neurotransmitters of the sensory, nociceptive system was reflected by increased CGRP and substance P content in the DRG and in the dorsal horn of the spinal cord. |
| 353 | 9743564 | No change of trkA receptor immunostaining was seen in DRGs of diabetic rats; however, a reduction of trkA immunoreactivity of DRG neurons was noted after long-term NGF treatment of healthy controls. |
| 354 | 9748608 | Stimulation of nerve growth-factor and substance P expression in the iris-trigeminal axis of diabetic rats--involvement of oxidative stress and effects of aldose reductase inhibition. |
| 355 | 9748608 | In rats with streptozotocin-induced diabetes, we measured increased (by 61%; P < 0.05) mRNA for nerve growth factor (NGF) in the iris together with increased (by 82%; P < 0.05) mRNA for preprotachykinin (the substance P precursor) in the trigeminal ganglion, suggesting that increased NGF was driving increased substance P gene expression. |
| 356 | 9748608 | Stimulation of nerve growth-factor and substance P expression in the iris-trigeminal axis of diabetic rats--involvement of oxidative stress and effects of aldose reductase inhibition. |
| 357 | 9748608 | In rats with streptozotocin-induced diabetes, we measured increased (by 61%; P < 0.05) mRNA for nerve growth factor (NGF) in the iris together with increased (by 82%; P < 0.05) mRNA for preprotachykinin (the substance P precursor) in the trigeminal ganglion, suggesting that increased NGF was driving increased substance P gene expression. |
| 358 | 9841517 | We measured the diameter of the basilar artery in vivo in nondiabetic and diabetic rats (streptozotocin, 50-60 mg/kg ip) in response to nitric oxide synthase-dependent agonists (acetylcholine and substance P) and a nitric oxide synthase-independent agonist (nitroglycerin). |
| 359 | 9865506 | -octane,chloride), all neurokinin (NK)1-receptor antagonists, SR-48,968 (S)-N-methyl-N[4-(4-acetylamino-4-[phenylpiperidino)-2-(3,4-dichlorophen yl)-butyl]benzamide, a tachykinin NK2 receptor antagonist and SR-142,801 (S)-(N)-(1-(3-(1-benzoyl-3-(3,4-dichlorophenyl) piperidin-3-yl)propyl)-4-phenylpiperidin-4-yl)-N-methyl acetamide, a tachykinin NK3 receptor antagonist, and of their respective inactive enantiomers on thresholds of vocalization due to a mechanical stimulus in mononeuropathic (sciatic nerve ligature) and diabetic rats, was examined. |
| 360 | 9865506 | The tachykinin NK1 and the NK2 receptor antagonists were antinociceptive in both models, with a higher effect of the former in diabetic rats. |
| 361 | 9865506 | -octane,chloride), all neurokinin (NK)1-receptor antagonists, SR-48,968 (S)-N-methyl-N[4-(4-acetylamino-4-[phenylpiperidino)-2-(3,4-dichlorophen yl)-butyl]benzamide, a tachykinin NK2 receptor antagonist and SR-142,801 (S)-(N)-(1-(3-(1-benzoyl-3-(3,4-dichlorophenyl) piperidin-3-yl)propyl)-4-phenylpiperidin-4-yl)-N-methyl acetamide, a tachykinin NK3 receptor antagonist, and of their respective inactive enantiomers on thresholds of vocalization due to a mechanical stimulus in mononeuropathic (sciatic nerve ligature) and diabetic rats, was examined. |
| 362 | 9865506 | The tachykinin NK1 and the NK2 receptor antagonists were antinociceptive in both models, with a higher effect of the former in diabetic rats. |
| 363 | 9934817 | The neuroendocrine peptides that we investigated were: secretin, gastric inhibitory polypeptide (GIP), gastrin, motilin, peptide YY (PYY), somatostatin, vasoactive intestinal polypeptide (VIP), substance P, neurotensin, neuropeptide Y (NPY) and galanin. |
| 364 | 9934817 | In the antrum, gastrin, somatostatin, VIP, substance P and NPY concentrations were significantly lower in obese diabetic mice than in the lean controls. |
| 365 | 9934817 | There was no statistical difference between the obese mice and lean controls for neurotensin and galanin content. |
| 366 | 9934817 | There was no statistical difference between obese diabetic mice and lean controls regarding the concentration of secretin, GIP, motilin, gastrin, somatostatin, VIP, neurotensin, NPY or galanin. |
| 367 | 9934817 | In the colon, the levels of PYY, somatostatin, VIP, substance P, NPY and galanin were significantly lower in the obese diabetic mice than the lean controls. |
| 368 | 9934817 | The neuroendocrine peptides that we investigated were: secretin, gastric inhibitory polypeptide (GIP), gastrin, motilin, peptide YY (PYY), somatostatin, vasoactive intestinal polypeptide (VIP), substance P, neurotensin, neuropeptide Y (NPY) and galanin. |
| 369 | 9934817 | In the antrum, gastrin, somatostatin, VIP, substance P and NPY concentrations were significantly lower in obese diabetic mice than in the lean controls. |
| 370 | 9934817 | There was no statistical difference between the obese mice and lean controls for neurotensin and galanin content. |
| 371 | 9934817 | There was no statistical difference between obese diabetic mice and lean controls regarding the concentration of secretin, GIP, motilin, gastrin, somatostatin, VIP, neurotensin, NPY or galanin. |
| 372 | 9934817 | In the colon, the levels of PYY, somatostatin, VIP, substance P, NPY and galanin were significantly lower in the obese diabetic mice than the lean controls. |
| 373 | 9934817 | The neuroendocrine peptides that we investigated were: secretin, gastric inhibitory polypeptide (GIP), gastrin, motilin, peptide YY (PYY), somatostatin, vasoactive intestinal polypeptide (VIP), substance P, neurotensin, neuropeptide Y (NPY) and galanin. |
| 374 | 9934817 | In the antrum, gastrin, somatostatin, VIP, substance P and NPY concentrations were significantly lower in obese diabetic mice than in the lean controls. |
| 375 | 9934817 | There was no statistical difference between the obese mice and lean controls for neurotensin and galanin content. |
| 376 | 9934817 | There was no statistical difference between obese diabetic mice and lean controls regarding the concentration of secretin, GIP, motilin, gastrin, somatostatin, VIP, neurotensin, NPY or galanin. |
| 377 | 9934817 | In the colon, the levels of PYY, somatostatin, VIP, substance P, NPY and galanin were significantly lower in the obese diabetic mice than the lean controls. |
| 378 | 10206182 | We studied the release of somatostatin, calcitonin gene-related peptide (CGRP) and substance P in response to electrical field stimulation from isolated tracheas of rats following 4 weeks of streptozotocin (50 mg/kg i.v.) |
| 379 | 10206182 | Field stimulation (40 V, 0.1 ms, 10 Hz for 120 s) increased the release of somatostatin, CGRP and substance P from the baseline 0.18+/-0.029, 0.17+/-0.027, and 1.77+/-0.086 to 0.51+/-0.022, 0.69+/-0.115, and 5.96+/-0.377 in control preparations and 0.31+/-0.081, 0.41+/-0.142, and 3.14+/-0.443 fmol/mg wet tissue weight in preparations from diabetic rats as measured by radioimmunoassay (control vs. diabetic P<0.01 for each). |
| 380 | 10206182 | We studied the release of somatostatin, calcitonin gene-related peptide (CGRP) and substance P in response to electrical field stimulation from isolated tracheas of rats following 4 weeks of streptozotocin (50 mg/kg i.v.) |
| 381 | 10206182 | Field stimulation (40 V, 0.1 ms, 10 Hz for 120 s) increased the release of somatostatin, CGRP and substance P from the baseline 0.18+/-0.029, 0.17+/-0.027, and 1.77+/-0.086 to 0.51+/-0.022, 0.69+/-0.115, and 5.96+/-0.377 in control preparations and 0.31+/-0.081, 0.41+/-0.142, and 3.14+/-0.443 fmol/mg wet tissue weight in preparations from diabetic rats as measured by radioimmunoassay (control vs. diabetic P<0.01 for each). |
| 382 | 10368989 | This study examines whether there is a change in the pattern of distribution of cholecystokinin-octapeptide (CCK-8), calcitonin-gene-related peptide (CGRP), neuropeptide-Y (NPY), substance P (SP) and vasoactive intestinal polypeptide (VIP) in the pancreas of streptozotocin (STZ)-diabetic (host) rats after subcutaneous pancreatic transplantation. |
| 383 | 10368989 | In conclusion, the pattern of distribution and density of NPY, SP and VIP in the pancreas of STZ-induced diabetic rats with SPTG is similar to that observed in normal pancreas, but the expression of CGRP and CCK-8 seemed to have increased as a result of transplantation and or diabetes. |
| 384 | 10374753 | In the present study, we show that prosaposin mRNA is significantly (p < 0.05) elevated in the peripheral nerve of streptozotocin-diabetic rats, a model of insulin-deficient diabetes in which nerve injury arises from the metabolic trauma of hyperglycemia and its consequences. |
| 385 | 10374753 | The dose-dependent prevention of nerve conduction slowing by TX 14(A) was accompanied by preservation of axonal caliber and sodium-potassium ATPase activity, while prevention of thermal hypoalgesia was associated with attenuation of the decline in nerve substance P levels. |
| 386 | 10395015 | Furthermore, this thermal allodynia and hyperalgesia in diabetic mice may be due to the enhanced release of substance P followed by activation of protein kinase C in the spinal cord. |
| 387 | 10440901 | Conversely, the mRNA expression of low-affinity neurotrophin receptor p75 was increased. |
| 388 | 10440901 | At birth, BDNF mRNA expression was affected with a significant generalized reduction,while in vibrissae we observed a reduction of BDNF and p75 mRNAs and an increase of NGF. |
| 389 | 10440901 | At postnatal day 14, pups from diabetic mothers showed reduced muscle levels of IGF-I, while we observed a partial impairment of substance P axonal transport at postnatal day 28. |
| 390 | 10440901 | In addition, these data suggest that nervous system abnormalities observed in diabetic embryopathy may also derive by insufficient neurotrophic factor biosynthesis involving sequentially NGF in the embryo and BDNF and IGF-I in the early postnatal days. |
| 391 | 10526098 | Substance P (SP) and calcitonin gene-related peptide (CGRP) constitute the main sensory peptides in the trigeminal ganglion (TG). |
| 392 | 10657496 | Distribution of calcitonin-gene-related peptide, neuropeptide-Y, vasoactive intestinal polypeptide, cholecystokinin-8, substance P and islet peptides in the pancreas of normal and diabetic rats. |
| 393 | 10657496 | This study investigates whether there is a change in the pattern of distribution of neuropeptides including calcitonin-gene-related peptide (CGRP), neuropeptide-Y (NPY), vasoactive intestinal polypeptide (VIP), cholecystokinin-octapeptide (CCK-8), substance P (SP), and islet peptides including insulin (INS), glucagon (GLU), somatostatin (SOM) and pancreatic polypeptide (PP) in the pancreas of streptozotocin (STZ)-diabetic rats. |
| 394 | 10657496 | After the onset of diabetes, the pattern of distribution of INS, GLU, SOM and PP cells was deranged. |
| 395 | 10657496 | In conclusion, CGRP, NPY, VIP, CCK-8 and SP are well distributed in both normal and diabetic pancreas. |
| 396 | 10657496 | Distribution of calcitonin-gene-related peptide, neuropeptide-Y, vasoactive intestinal polypeptide, cholecystokinin-8, substance P and islet peptides in the pancreas of normal and diabetic rats. |
| 397 | 10657496 | This study investigates whether there is a change in the pattern of distribution of neuropeptides including calcitonin-gene-related peptide (CGRP), neuropeptide-Y (NPY), vasoactive intestinal polypeptide (VIP), cholecystokinin-octapeptide (CCK-8), substance P (SP), and islet peptides including insulin (INS), glucagon (GLU), somatostatin (SOM) and pancreatic polypeptide (PP) in the pancreas of streptozotocin (STZ)-diabetic rats. |
| 398 | 10657496 | After the onset of diabetes, the pattern of distribution of INS, GLU, SOM and PP cells was deranged. |
| 399 | 10657496 | In conclusion, CGRP, NPY, VIP, CCK-8 and SP are well distributed in both normal and diabetic pancreas. |
| 400 | 10718343 | Functional HGF receptors were deed in MMC by HGF-induced extracellular acidification, a response that was inhibited by the HGF inhibitor HGF/NK2, a splice variant expressing the N-terminal domain through the second kringle domain HGF also increased fibronectin and collagen alpha1 (IV) mRNA levels in these cells; the increases were associated with a concentration-dependent increase in transcriptional activity of the collagen alpha1 (IV) gene. |
| 401 | 10718343 | HGF also stimulated fibronectin and collagen alpha1 (IV) mRNA levels in primary rabbit proximal tubule epithelial cells To evaluate the potential consequences of chronic elevation of HGF on renal fuction, HGF was administered continuously for 18 days to normal and diabetic C57BLKS/J lepr(db) mice. |
| 402 | 10884525 | The tachykinin NK(1) receptor antagonist (S)-1-[2-[3-(3, 4-dichlorophenyl)-1 (3-isopropoxyphenylacetyl)piperidin-3-yl] ethyl]-4-phenyl-1 azoniabicyclo [2.2.2]octane cloride (SR140333; 120 nmol/kg, s.c.+120 nmol/kg, i.v.) significantly inhibited plasma exudation and paw oedema evoked by staphylococcal enterotoxin B. |
| 403 | 10884525 | The tachykinin NK(2) receptor antagonist (S)-N-methyl-N[4-(4-acetylamino-4-phenyl piperidino)-2-(3, 4-dichlorophenyl)butyl]-benzamide (SR48968) had no effect on the staphylococcal enterotoxin B-induced responses. |
| 404 | 10884525 | The 5-HT receptor antagonist methysergide (10 mg/kg, i.v.) and the histamine H(1) receptor antagonist mepyramine (10 mg/kg, i.v.) produced a significant reduction in paw oedema whereas plasma exudation was reduced only by methysergide. |
| 405 | 10915836 | A tachykinin NK(1) receptor antagonist, RP-67,580 ((3aR,7aR) -7, 7-diphenyl-2-(1-imino-2(2-methoxy phenyl)-ethyl) perhydroisoindol-4-one hydrochloride), a tachykinin NK(2) receptor antagonist, SR-48,968 ((S)-N-methyl (4-(acetylamino-4phenylpiperidino)-2-(3, 4-dichlorophenyl) butyl) benzamide) and their respective enantiomers were intrathecally administered 4 weeks after the induction of diabetes. |
| 406 | 11179603 | Distribution of vasoactive intestinal polypeptide, neuropeptide-Y and substance P and their effects on insulin secretion from the in vitro pancreas of normal and diabetic rats. |
| 407 | 11179603 | This study examined the pattern of distribution of vasoactive intestinal polypeptide (VIP), neuropeptide-Y (NPY) and substance P (SP) in the pancreas of diabetic rat to determine whether there are changes in the number and pattern of distribution of these neuropeptides after the onset of diabetes. |
| 408 | 11179603 | Moreover, the effect of VIP, NPY and SP on insulin secretion from the pancreas of normal and diabetic rats was also examined. |
| 409 | 11179603 | The number of insulin-positive cells in the islets of Langerhans was reduced while that of VIP and NPY increased significantly after the onset of diabetes. |
| 410 | 11179603 | NPY also induced a marked (P < 0.005) increase in insulin release from pancreatic tissue fragments of normal rat. |
| 411 | 11179603 | Stimulation of pancreatic tissue fragments of diabetic rat with NPY resulted in a slight but not significant increase in insulin release. |
| 412 | 11179603 | In summary, VIP and NPY can stimulate insulin secretion from the pancreas after the onset of diabetes. |
| 413 | 11179603 | Distribution of vasoactive intestinal polypeptide, neuropeptide-Y and substance P and their effects on insulin secretion from the in vitro pancreas of normal and diabetic rats. |
| 414 | 11179603 | This study examined the pattern of distribution of vasoactive intestinal polypeptide (VIP), neuropeptide-Y (NPY) and substance P (SP) in the pancreas of diabetic rat to determine whether there are changes in the number and pattern of distribution of these neuropeptides after the onset of diabetes. |
| 415 | 11179603 | Moreover, the effect of VIP, NPY and SP on insulin secretion from the pancreas of normal and diabetic rats was also examined. |
| 416 | 11179603 | The number of insulin-positive cells in the islets of Langerhans was reduced while that of VIP and NPY increased significantly after the onset of diabetes. |
| 417 | 11179603 | NPY also induced a marked (P < 0.005) increase in insulin release from pancreatic tissue fragments of normal rat. |
| 418 | 11179603 | Stimulation of pancreatic tissue fragments of diabetic rat with NPY resulted in a slight but not significant increase in insulin release. |
| 419 | 11179603 | In summary, VIP and NPY can stimulate insulin secretion from the pancreas after the onset of diabetes. |
| 420 | 11284388 | In addition to, but independent of its serine type catalytic activity, DPPIV binds closely to the soluble extracellular enzyme adenosine deaminase. |
| 421 | 11284388 | Other known substrates which are subject in vitro to receptor-specific changes induced by DPPIV truncation include neuropeptides such as substance P, peptidE YY and neuropeptide Y. |
| 422 | 11284388 | On the other hand, DPPIV mediated cleavage of the N-terminal His-Ala or Tyr-Ala dipeptides from circulating incretin hormones like, glucagon-like peptides (GLP)-1 and -2, gastric inhibitory polypeptide (GIP), all members of the enteroglucagon/GRF superfamily, results in their biological inactivation in vitro and in vivo. |
| 423 | 11284388 | Administration of specific DPPIV inhibitors closes this pathway of incretin degradation and greatly enhances insulin secretion. |
| 424 | 11446269 | Angiotensin-converting enzyme (ACE) inhibitors, widely and successfully used in the treatment of hypertension, may also provide renal protection independent of blood pressure reduction; however, their relatively nonspecific mode of action in blocking an early metabolic step entails major clinical disadvantages, such as accumulation of bradykinin and substance P, that may cause the characteristic ACE-inhibitor side effects of persistent dry cough and, more rarely, angioneurotic edema. |
| 425 | 11446269 | Angiotensin II antagonists or receptor blockers, a new class of antihypertensive agent, selectively antagonize the AT1 receptor subtype and, because of greater specificity, do not give rise to the side effects associated with ACE inhibitors. |
| 426 | 11768246 | Selected important clinical learning points include the following: (1) glutamine may restore the AIDs-associated increased intestinal permeability to normal; (2) substance P is a major mediator of diarrhea caused by Costridium difficile toxin A, acting by binding to a G-protein-coupled receptor, and represents a possible 2therapeutic target; (3) the serological diagnosis of celiac disease has been greatly enhanced with the use of anti-endomysial antibody testing, and the recent antitransglutaminase; (4) a quarter of patients with celiac disease may have secondary pancreatic insufficiency and require enzyme replacement therapy; (5) in the patient with unexplained elevation in the serum transaminase concentration, consider celiac disease as an obscure possibility; (6) bosentan and endothelin receptor agonist may prove to be useful in reducing gut ischemia in patients with septic shock; and (7) the administration of recombinant human fibroblast growth factor-2 may prove to be useful to prevent radiation damage to the gastrointestinal tract. |
| 427 | 11943667 | The organ fluid of the preparations were also tested for substance P, calcitonin gene-related peptide (CGRP), and somatostatin concentrations by RIA. |
| 428 | 11943667 | Exogenous CGRP and substance P potentiated, whereas somatostatin inhibited (1 nM-10 microM) the FS-induced contractions in rings from either group. |
| 429 | 11943667 | FS released somatostatin, CGRP, and substance P from 0.17 +/- 0.024, 0.15 +/- 0.022, and 1.65 +/- 0.093 to 0.58 +/- 0.032, 0.74 +/- 0.122, and 5.34 +/- 0.295 in preparations from normal, and from 0.19 +/- 0.016, 0.11 +/- 0.019, and 0.98 +/- 0.116 to 0.22 +/- 0.076, 0.34 +/- 0.099, and 1.84 +/- 0.316 fmol/mg wet wt in preparations from diabetic rats. |
| 430 | 11943667 | The organ fluid of the preparations were also tested for substance P, calcitonin gene-related peptide (CGRP), and somatostatin concentrations by RIA. |
| 431 | 11943667 | Exogenous CGRP and substance P potentiated, whereas somatostatin inhibited (1 nM-10 microM) the FS-induced contractions in rings from either group. |
| 432 | 11943667 | FS released somatostatin, CGRP, and substance P from 0.17 +/- 0.024, 0.15 +/- 0.022, and 1.65 +/- 0.093 to 0.58 +/- 0.032, 0.74 +/- 0.122, and 5.34 +/- 0.295 in preparations from normal, and from 0.19 +/- 0.016, 0.11 +/- 0.019, and 0.98 +/- 0.116 to 0.22 +/- 0.076, 0.34 +/- 0.099, and 1.84 +/- 0.316 fmol/mg wet wt in preparations from diabetic rats. |
| 433 | 11943667 | The organ fluid of the preparations were also tested for substance P, calcitonin gene-related peptide (CGRP), and somatostatin concentrations by RIA. |
| 434 | 11943667 | Exogenous CGRP and substance P potentiated, whereas somatostatin inhibited (1 nM-10 microM) the FS-induced contractions in rings from either group. |
| 435 | 11943667 | FS released somatostatin, CGRP, and substance P from 0.17 +/- 0.024, 0.15 +/- 0.022, and 1.65 +/- 0.093 to 0.58 +/- 0.032, 0.74 +/- 0.122, and 5.34 +/- 0.295 in preparations from normal, and from 0.19 +/- 0.016, 0.11 +/- 0.019, and 0.98 +/- 0.116 to 0.22 +/- 0.076, 0.34 +/- 0.099, and 1.84 +/- 0.316 fmol/mg wet wt in preparations from diabetic rats. |
| 436 | 12025969 | Changes in responsiveness of the vas deferens and urinary bladder to bradykinin (BK) receptor agonists (Tyr8-BK and des-Arg9-BK), substance P (SP), and endothelin-1 (ET-1) were assessed 8 weeks after streptozotocin (STZ)-induced diabetes. |
| 437 | 12025969 | Insulin treatment of nondiabetic rats, however, also affected VD (but not UB) responsiveness, such that contractions to Tyr8-BK and TP by ET-1 were increased, but TP by Tyr8-BK was decreased. |
| 438 | 12406165 | Neutral endopeptidase (NEP), a cell surface metallopeptidase, degrades substance P. |
| 439 | 12437489 | Both angiotensin-converting enzyme (ACE) inhibitors and AT-1 receptor antagonists reduce the effects of angiotensin II, however they may have different clinical effects. |
| 440 | 12437489 | This is because the ACE inhibitors, but not the AT-1 receptor antagonists, increase the levels of substance P, bradykinin and tissue plasminogen activator. |
| 441 | 12437489 | The AT-1 receptor antagonists, but not the ACE inhibitors, are capable of inhibiting the effects of angiotensin II produced by enzymes other than ACE. |
| 442 | 12449521 | This study investigated the time-course of the nociceptive neuropeptide substance P and nerve growth factor (NGF), which facilitates substance P production, in lumbar and cervical dorsal root ganglia (DRG) of streptozotocin-induced diabetic rats. |
| 443 | 12449521 | Levels of substance P and NGF were measured by radioimmunoassay and sandwich enzyme-linked immunosorbent assay, respectively, 2 months, 4 months and 8 months after induction of diabetes, and compared with age-matched non-diabetic control rats. |
| 444 | 12449521 | At 2 months and 4 months, substance P and NGF levels were lower in the lumbar DRG of the diabetic rats than in controls. |
| 445 | 12449521 | At 8 months, substance P and NGF were lower in both the lumbar and cervical DRG of the diabetic rats than in controls. |
| 446 | 12449521 | These data demonstrate that a decrease in substance P levels in primary sensory neurons with NGF depletion occurs in an axonal length-dependent manner in diabetic rats, and that this decrease may be correlated with the duration of diabetes. |
| 447 | 12449521 | This study investigated the time-course of the nociceptive neuropeptide substance P and nerve growth factor (NGF), which facilitates substance P production, in lumbar and cervical dorsal root ganglia (DRG) of streptozotocin-induced diabetic rats. |
| 448 | 12449521 | Levels of substance P and NGF were measured by radioimmunoassay and sandwich enzyme-linked immunosorbent assay, respectively, 2 months, 4 months and 8 months after induction of diabetes, and compared with age-matched non-diabetic control rats. |
| 449 | 12449521 | At 2 months and 4 months, substance P and NGF levels were lower in the lumbar DRG of the diabetic rats than in controls. |
| 450 | 12449521 | At 8 months, substance P and NGF were lower in both the lumbar and cervical DRG of the diabetic rats than in controls. |
| 451 | 12449521 | These data demonstrate that a decrease in substance P levels in primary sensory neurons with NGF depletion occurs in an axonal length-dependent manner in diabetic rats, and that this decrease may be correlated with the duration of diabetes. |
| 452 | 12449521 | This study investigated the time-course of the nociceptive neuropeptide substance P and nerve growth factor (NGF), which facilitates substance P production, in lumbar and cervical dorsal root ganglia (DRG) of streptozotocin-induced diabetic rats. |
| 453 | 12449521 | Levels of substance P and NGF were measured by radioimmunoassay and sandwich enzyme-linked immunosorbent assay, respectively, 2 months, 4 months and 8 months after induction of diabetes, and compared with age-matched non-diabetic control rats. |
| 454 | 12449521 | At 2 months and 4 months, substance P and NGF levels were lower in the lumbar DRG of the diabetic rats than in controls. |
| 455 | 12449521 | At 8 months, substance P and NGF were lower in both the lumbar and cervical DRG of the diabetic rats than in controls. |
| 456 | 12449521 | These data demonstrate that a decrease in substance P levels in primary sensory neurons with NGF depletion occurs in an axonal length-dependent manner in diabetic rats, and that this decrease may be correlated with the duration of diabetes. |
| 457 | 12449521 | This study investigated the time-course of the nociceptive neuropeptide substance P and nerve growth factor (NGF), which facilitates substance P production, in lumbar and cervical dorsal root ganglia (DRG) of streptozotocin-induced diabetic rats. |
| 458 | 12449521 | Levels of substance P and NGF were measured by radioimmunoassay and sandwich enzyme-linked immunosorbent assay, respectively, 2 months, 4 months and 8 months after induction of diabetes, and compared with age-matched non-diabetic control rats. |
| 459 | 12449521 | At 2 months and 4 months, substance P and NGF levels were lower in the lumbar DRG of the diabetic rats than in controls. |
| 460 | 12449521 | At 8 months, substance P and NGF were lower in both the lumbar and cervical DRG of the diabetic rats than in controls. |
| 461 | 12449521 | These data demonstrate that a decrease in substance P levels in primary sensory neurons with NGF depletion occurs in an axonal length-dependent manner in diabetic rats, and that this decrease may be correlated with the duration of diabetes. |
| 462 | 12449521 | This study investigated the time-course of the nociceptive neuropeptide substance P and nerve growth factor (NGF), which facilitates substance P production, in lumbar and cervical dorsal root ganglia (DRG) of streptozotocin-induced diabetic rats. |
| 463 | 12449521 | Levels of substance P and NGF were measured by radioimmunoassay and sandwich enzyme-linked immunosorbent assay, respectively, 2 months, 4 months and 8 months after induction of diabetes, and compared with age-matched non-diabetic control rats. |
| 464 | 12449521 | At 2 months and 4 months, substance P and NGF levels were lower in the lumbar DRG of the diabetic rats than in controls. |
| 465 | 12449521 | At 8 months, substance P and NGF were lower in both the lumbar and cervical DRG of the diabetic rats than in controls. |
| 466 | 12449521 | These data demonstrate that a decrease in substance P levels in primary sensory neurons with NGF depletion occurs in an axonal length-dependent manner in diabetic rats, and that this decrease may be correlated with the duration of diabetes. |
| 467 | 12485446 | The cell surface enzyme, neutral endopeptidase, degrades substance P, thereby regulating its biologic actions. |
| 468 | 12602781 | The neuroendocrine peptides known to regulate gastrointestinal motility, namely secretin, gastric inhibitory peptide (GIP), motilin, somatostatin, peptide YY (PYY), substance P, vasoactive intestinal polypeptide (VIP) and galanin, were measured in tissue extracts of different segments of the gut by radioimmunoassay. |
| 469 | 12602781 | The concentrations of antral somatostatin, VIP and galanin, and duodenal secretin as well as jejunal motilin in NOD mice were higher than those of controls. |
| 470 | 12602781 | Duodenal GIP and colonic PYY concentration in NOD mice was lower than controls. |
| 471 | 12602781 | Duodenal GIP and VIP, and colonic somatostatin and VIP levels were lower in obese diabetic mice than controls. |
| 472 | 12602781 | Whereas the high concentrations of antral VIP and galanin and the low level of colonic PYY in diabetic NOD mice may contribute to the development of diarrhea in NOD mice, the decreased levels of duodenal and colonic VIP and colonic somatostatin in obese diabetic mice may account for the constipation encountered in these animals. |
| 473 | 12602782 | Whereas the contents of peptide YY (PYY) and somatostatin were higher in obese diabetic mice, the contents of substance P and VIP were lower. |
| 474 | 12602782 | The changes in the colonic contents of PYY, VIP and somatostatin may cause low intestinal secretion and, together with slow GIT, give rise to constipation, which is a common symptom in diabetes. |
| 475 | 12764579 | Promotion of corneal epithelial wound healing in diabetic rats by the combination of a substance P-derived peptide (FGLM-NH2) and insulin-like growth factor-1. |
| 476 | 14555187 | Contractions to capsaicin (30 nM and 1 microM) were resistant to tetrodotoxin, strongly reduced by a combination of tachykinin NK(1) and NK(2) receptor antagonists, and slightly reduced in preparations from diabetic animals. |
| 477 | 14668049 | The best studied of the neurotrophic factors is nerve growth factor (NGF) and the related members of the neurotrophin family of peptides. |
| 478 | 14668049 | There is increasing evidence that there is a deficiency of NGF in diabetes, as well as the dependent neuropeptides substance P (SP) and calcitonin gene-related peptide (CGRP) that may also contribute to the clinical symptoms resulting from small fiber dysfunction. |
| 479 | 15093698 | In the present study on 18 GK rats and 21 control Wistar rats, the occurrence of the sensory neuropeptides substance P (SP) and calcitonin gene-related peptide (CGRP), and the autonomic neuropeptide Y (NPY) was analysed in bone and joints, dorsal root ganglia and lumbar spinal cord by immunohistochemistry and radioimmunoassay (RIA). |
| 480 | 15093698 | While SP, CGRP and NPY in periosteum, cortical bone and synovium was confined to neuronal tissue, the bone marrow in addition exhibited an abundance of NPY-positive megakaryocytes. |
| 481 | 15093698 | Given the suggested anabolic role of NPY and CGRP on bone, neuropeptidergic deficit in diabetes may prove to be an important factor underlying the development of regional osteopenia. |
| 482 | 15448099 | To evaluate the possible role of neuropeptide immunoreactive primary sensory neurons on the development of nociceptive dysfunction in diabetes, the absolute numbers of immunoreactive substance P and calcitonin gene-related peptide (CGRP) dorsal root ganglion (DRG) cell bodies were estimated in diabetic and nondiabetic BALB/C (p75(+/+)) and p75 receptor knockout (p75(-/-)) mice with unilateral sciatic nerve crush. |
| 483 | 15448099 | The total numbers of immunoreactive substance P A-cells, substance P B-cells, CGRP A-cells, and CGRP B-cells in L5DRG were estimated using semithick consecutive sections and the optical fractionator. |
| 484 | 15448099 | In p75(+/+) and p75(-/-) mice, there was no effect of diabetes on the immunoreactive CGRP B-cell number, nor was there any effect of diabetes on the immunoreactive substance P B-cell number. |
| 485 | 15448099 | It is concluded that experimental diabetes in the mouse is associated with loss of immunoreactive CGRP primary sensory neurons of the A-cell phenotype, that this loss could play a role for the touch-evoked nociception in the model, and that the neuronal immunoreactive CGRP abnormality possibly is mediated by activation of the p75 neurotrophin receptor. |
| 486 | 15448099 | To evaluate the possible role of neuropeptide immunoreactive primary sensory neurons on the development of nociceptive dysfunction in diabetes, the absolute numbers of immunoreactive substance P and calcitonin gene-related peptide (CGRP) dorsal root ganglion (DRG) cell bodies were estimated in diabetic and nondiabetic BALB/C (p75(+/+)) and p75 receptor knockout (p75(-/-)) mice with unilateral sciatic nerve crush. |
| 487 | 15448099 | The total numbers of immunoreactive substance P A-cells, substance P B-cells, CGRP A-cells, and CGRP B-cells in L5DRG were estimated using semithick consecutive sections and the optical fractionator. |
| 488 | 15448099 | In p75(+/+) and p75(-/-) mice, there was no effect of diabetes on the immunoreactive CGRP B-cell number, nor was there any effect of diabetes on the immunoreactive substance P B-cell number. |
| 489 | 15448099 | It is concluded that experimental diabetes in the mouse is associated with loss of immunoreactive CGRP primary sensory neurons of the A-cell phenotype, that this loss could play a role for the touch-evoked nociception in the model, and that the neuronal immunoreactive CGRP abnormality possibly is mediated by activation of the p75 neurotrophin receptor. |
| 490 | 15448099 | To evaluate the possible role of neuropeptide immunoreactive primary sensory neurons on the development of nociceptive dysfunction in diabetes, the absolute numbers of immunoreactive substance P and calcitonin gene-related peptide (CGRP) dorsal root ganglion (DRG) cell bodies were estimated in diabetic and nondiabetic BALB/C (p75(+/+)) and p75 receptor knockout (p75(-/-)) mice with unilateral sciatic nerve crush. |
| 491 | 15448099 | The total numbers of immunoreactive substance P A-cells, substance P B-cells, CGRP A-cells, and CGRP B-cells in L5DRG were estimated using semithick consecutive sections and the optical fractionator. |
| 492 | 15448099 | In p75(+/+) and p75(-/-) mice, there was no effect of diabetes on the immunoreactive CGRP B-cell number, nor was there any effect of diabetes on the immunoreactive substance P B-cell number. |
| 493 | 15448099 | It is concluded that experimental diabetes in the mouse is associated with loss of immunoreactive CGRP primary sensory neurons of the A-cell phenotype, that this loss could play a role for the touch-evoked nociception in the model, and that the neuronal immunoreactive CGRP abnormality possibly is mediated by activation of the p75 neurotrophin receptor. |
| 494 | 15574134 | The numbers of substance P (SP) and vasoactive intestinal polypeptide IR perikarya were also increased by insulin treatment. |
| 495 | 15869864 | Expression of the NK-1 receptor on islet cells and invading immune cells in the non-obese diabetic mouse. |
| 496 | 15869864 | Substance P (SP) is a substance known to have pro-inflammatory, endocrine, neuromodulatory and trophic effects, and its preferred receptor, the neurokinin receptor 1 (NK-1 R), is reported to be involved in extravasation of granulocytes and in inflammation and tissue derangement. |
| 497 | 15907807 | In this paper, we report on (1) the kinetics of binding, (2) the type of inhibition, (3) the selectivity with respect to other peptidases, and (4) the inhibitory potency on the DPP IV catalyzed degradation of glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP) and substance P. |
| 498 | 15907807 | It is a micromolar inhibitor for dipeptidyl-peptidase 8 and does not significantly inhibit dipeptidyl-peptidase II (EC 3.4.11.2), prolyl oligopeptidase (EC 3.4.21.26), aminopeptidase P (EC 3.4.11.9) or aminopeptidase M (EC 3.4.11.2). |
| 499 | 15907807 | There was no evidence for substrate specific inhibition of DPP IV by Vildagliptin or for important allosteric factors affecting the inhibition constant in presence of GIP and GLP-1. |
| 500 | 16199188 | Substance P is one of the neurotransmitters released by primary nociceptive neurons in the dorsal horn of the spinal cord and it binds postsynaptically to NK(1)-receptors. |
| 501 | 16199188 | The aim of this multicenter, randomised, double-blind, placebo-controlled and parallel-group study was to test if the non-peptide NK(1)-receptor antagonist TKA731 would relieve painful diabetic polyneuropathy. |
| 502 | 16427624 | Once the disease progressed into its more severe stages, NGF, although still capable of altering the electrophysiological profile of the sensory A- and C-fibers and influencing the expression of p75 and substance P in the dorsal root ganglia, could no longer maintain normal nociception. |
| 503 | 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. |
| 504 | 17174891 | Delivering the neuropeptide substance P by intra-arterial injection into the NOD pancreas reverses abnormal insulin resistance, insulitis, and diabetes for weeks. |
| 505 | 17704566 | Structural studies of a bifunctional inhibitor of neprilysin and DPP-IV. |
| 506 | 17704566 | Neutral endopeptidase (NEP) is the major enzyme involved in the metabolic inactivation of a number of bioactive peptides including the enkephalins, substance P, endothelin, bradykinin and atrial natriuretic factor, as well as the incretin hormone glucagon-like peptide 1 (GLP-1), which is a potent stimulator of insulin secretion. |
| 507 | 17704566 | The activity of GLP-1 is also rapidly abolished by the serine protease dipeptidyl peptidase IV (DPP-IV), which led to an elevated interest in inhibitors of this enzyme for the treatment of type II diabetes. |
| 508 | 17928748 | Capsaicin (10 microM), substance P (SP 2 microM) and neurokinin A (NKA 2 microM) caused a transient increase in MI in both control and STZ-induced diabetic rats. |
| 509 | 18025295 | Bradykinin and substance P, substrates of angiotensin-converting enzyme, increase vascular permeability and cause tissue edema in animals. |
| 510 | 18025295 | Studies indicate that amino-terminal degradation of these peptides, by aminopeptidase P and dipeptidyl peptidase IV, may be impaired in individuals with angiotensin-converting enzyme inhibitor-associated angioedema. |
| 511 | 18025295 | Sera were assayed for angiotensin-converting enzyme activity, aminopeptidase P activity, aminopeptidase N activity, dipeptidyl peptidase IV activity, and antigen and the ex vivo degradation half-lives of bradykinin, des-Arg(9)-bradykinin, and substance P in a subset. |
| 512 | 18025295 | The degradation half-life of substance P correlated inversely with dipeptidyl peptidase IV antigen during angiotensin-converting enzyme inhibition. |
| 513 | 18025295 | Bradykinin and substance P, substrates of angiotensin-converting enzyme, increase vascular permeability and cause tissue edema in animals. |
| 514 | 18025295 | Studies indicate that amino-terminal degradation of these peptides, by aminopeptidase P and dipeptidyl peptidase IV, may be impaired in individuals with angiotensin-converting enzyme inhibitor-associated angioedema. |
| 515 | 18025295 | Sera were assayed for angiotensin-converting enzyme activity, aminopeptidase P activity, aminopeptidase N activity, dipeptidyl peptidase IV activity, and antigen and the ex vivo degradation half-lives of bradykinin, des-Arg(9)-bradykinin, and substance P in a subset. |
| 516 | 18025295 | The degradation half-life of substance P correlated inversely with dipeptidyl peptidase IV antigen during angiotensin-converting enzyme inhibition. |
| 517 | 18025295 | Bradykinin and substance P, substrates of angiotensin-converting enzyme, increase vascular permeability and cause tissue edema in animals. |
| 518 | 18025295 | Studies indicate that amino-terminal degradation of these peptides, by aminopeptidase P and dipeptidyl peptidase IV, may be impaired in individuals with angiotensin-converting enzyme inhibitor-associated angioedema. |
| 519 | 18025295 | Sera were assayed for angiotensin-converting enzyme activity, aminopeptidase P activity, aminopeptidase N activity, dipeptidyl peptidase IV activity, and antigen and the ex vivo degradation half-lives of bradykinin, des-Arg(9)-bradykinin, and substance P in a subset. |
| 520 | 18025295 | The degradation half-life of substance P correlated inversely with dipeptidyl peptidase IV antigen during angiotensin-converting enzyme inhibition. |
| 521 | 18378339 | The protein and mRNA expression of TRPV1, calcitonin gene-related peptide (CGRP) and substance P (SP) levels in hearts were measured, respectively. |
| 522 | 18378339 | Compared with control mice, blood glucose was significantly increased in diabetic mice (P<0.05), while the protein and mRNA expression of TRPV1, CGRP and SP levels in hearts were essentially reduced in diabetic mice (P<0.05). |
| 523 | 18378339 | TRPV1 and its main neuropeptides, CGRP and SP, in hearts were impaired during DM. |
| 524 | 18550223 | Substance P and secretoneurin in vitreous aspirates of patients with various vitreoretinal diseases. |
| 525 | 18550223 | By means of highly sensitive radioimmunoassays, the levels of substance P (SP) and secretoneurin (SN) were detected in vitreous aspirates of patients with macular holes which served as controls, in patients with nonproliferative diabetic retinopathy (DR), active proliferative diabetic retinopathy (active PDR), inactive PDR, rhegmatogenous retinal detachment and proliferative vitreoretinopathy (PVR). |
| 526 | 18550223 | Substance P and secretoneurin in vitreous aspirates of patients with various vitreoretinal diseases. |
| 527 | 18550223 | By means of highly sensitive radioimmunoassays, the levels of substance P (SP) and secretoneurin (SN) were detected in vitreous aspirates of patients with macular holes which served as controls, in patients with nonproliferative diabetic retinopathy (DR), active proliferative diabetic retinopathy (active PDR), inactive PDR, rhegmatogenous retinal detachment and proliferative vitreoretinopathy (PVR). |
| 528 | 18776996 | After induction of differentiation, HAEC expressed multiple pancreatic beta-cell genes, including insulin, pancreas duodenum homeobox-1, paired box gene 6, NK2 transcription factor-related locus 2, Islet 1, glucokinase, and glucose transporter-2, and released C-peptide in a glucose-regulated manner in response to other extracellular stimulations. |
| 529 | 19283667 | We used immunohistochemistry to investigate collagen protein expression as a marker for tissue remodelling together with endothelial nitric oxide synthase (eNOS) protein expression as a marker for endothelial-dependent vasodilation. |
| 530 | 19283667 | Our results revealed that A) Diabetic myocardium appears more vulnerable to ischemia/reperfusion injury than normal myocardium with regard to myocardial interstitium and microvessel ultrastructure, as well as eNOS protein expression; B) Inflammation response increases in diabetic animals exposed to ischemia/reperfusion injury compared to controls; C) Pre-treatment of diabetic myocardium with EGb results in an improvement of impaired endothelial-dependent vasodilation in diabetes and additional ischemia/ reperfusion, diminished mast cell and substance P accumulation, and better preserved myocardial ultrastructure compared to unprotected myocardium. |
| 531 | 19295489 | Substance P (SP), a sensory nerve derived neuropeptide, has been implicated in wound repair. |
| 532 | 19295489 | Using a 2% agarose gel, immortalized human microvascular endothelial cells (HMEC-1) were plated into a 1.5-mm well, and agonist (SP; 10(-4) mol/L) was loaded into a 3-mm well; controls included NaCl, albumin (bovine serum albumin), and vascular endothelial cell growth factor. |
| 533 | 19295489 | Human microvascular endothelial cell 1 migration toward the SP exceeded NaCl or bovine serum albumin; vascular endothelial cell growth factor had similar effects. |
| 534 | 19816194 | We hypothesized that nerve growth factor (NGF), which enhances the expression of key mediators of nociception (i.e. substance P [SP] and calcitonin gene-related peptide), contributes to the development of mechanical allodynia in these mice. |
| 535 | 19836387 | We observed that this heptapeptide induced a dose-dependent inhibitory effect on the substance P-induced response, which was reversible by the non-selective opioid receptor antagonist naloxone. |
| 536 | 19847599 | Efficacy of substance P and insulin-like growth factor-1 peptides for preventing postsurgical superficial punctate keratopathy in diabetic patients. |
| 537 | 20070982 | To achieve this goal, the effect of diabetes on wound healing, along with the role of inflammatory cytokines such as interleukin-6 (IL-6) and interleukin-8 (IL-8) secreted in the wound microenvironment, and neuropeptides such as substance P (SP) and neuropeptide Y (NPY), secreted from peripheral nerves is monitored in non-diabetic and diabetic rabbits. |
| 538 | 20070982 | Diabetic rabbits show significantly increased baseline gene expression of IL-6 and IL-8, their receptors, CXCR1, CXCR2, GP-130, and a decrease of prepro tachykinin-A (PP-TA), the precursor of SP, whereas the expression of prepro-NPY (PP-NPY), the precursor of NPY is not different. |
| 539 | 20070982 | Post-injury, the increase over baseline gene expression of IL-6, IL-8, CXCR1, CXCR2, and GP-130 is significantly less in diabetic wounds compared with non-diabetic wounds. |
| 540 | 20457219 | The hyperglycemic and hyperinsulinemic effects of the TRH analog in the RVLM was peptide specific, since angiotensin II or a substance P analog at the same dose had weak or no effects. |
| 541 | 20490673 | Nerve growth factor and substance P: expression in a rat model of diabetic bladder. |
| 542 | 20832942 | Basal and stimulated release of calcitonin gene-related peptide (CGRP), Substance P (SP) and prostaglandin E(2) (PGE(2)) from isolated skin and sciatic nerve were assessed by enzyme immunoassays. |
| 543 | 20933559 | The antinociceptive effect of substance P(1-7) amide was reversed by naloxone but not by the selective opioid receptor antagonist β-funaltrexamine, naltrindole or nor-binaltorphimine, selective for the μ-, δ- or κ-opioid receptor, respectively. |
| 544 | 21036226 | Modulation of the constitutive activity of the ghrelin receptor by use of pharmacological tools and mutagenesis. |
| 545 | 21036226 | The ghrelin receptor is characterized by an ability to signal even without any ligand present with approximately 50% of the maximally ghrelin-induced efficacy-a feature that may have important physiological implications. |
| 546 | 21036226 | [D-Arg(1), D-Phe(5), D-Trp(7,9), Leu(11)]-substance P was the first inverse agonist to be identified for the ghrelin receptor, and this peptide has been used as a starting point for identification of the structural requirements for inverse agonist properties in the ligand. |
| 547 | 21036226 | It is suggested that inverse agonist and antagonist against the ghrelin receptor provide an interesting possibility in the development of drugs for treatment of obesity and diabetes and that improved structural understanding of the receptor function facilitates the drug development. |
| 548 | 21389974 | Hematopoietic growth factor inducible neurokinin-1 (Gpnmb/Osteoactivin) is a biomarker of progressive renal injury across species. |
| 549 | 21389974 | We sought to find a urinary biomarker for chronic kidney disease and tested hematopoietic growth factor inducible neurokinin-1 (HGFIN, also known as Gpnmb/Osteoactivin) as it was found to be a kidney injury biomarker in microarray studies. |
| 550 | 21389974 | The urine HGFIN-to-creatinine ratio compared favorably with the urine neutrophil gelatinase-associated lipocalin (NGAL)-to-creatinine ratio (both measured by commercial enzyme-linked immunosorbent assays (ELISAs)), and correlated strongly with proteinuria, but weakly with estimated glomerular filtration rate and serum creatinine. |
| 551 | 21389974 | Hematopoietic growth factor inducible neurokinin-1 (Gpnmb/Osteoactivin) is a biomarker of progressive renal injury across species. |
| 552 | 21389974 | We sought to find a urinary biomarker for chronic kidney disease and tested hematopoietic growth factor inducible neurokinin-1 (HGFIN, also known as Gpnmb/Osteoactivin) as it was found to be a kidney injury biomarker in microarray studies. |
| 553 | 21389974 | The urine HGFIN-to-creatinine ratio compared favorably with the urine neutrophil gelatinase-associated lipocalin (NGAL)-to-creatinine ratio (both measured by commercial enzyme-linked immunosorbent assays (ELISAs)), and correlated strongly with proteinuria, but weakly with estimated glomerular filtration rate and serum creatinine. |
| 554 | 21467195 | Substance P (SP)-neurokinin-1 receptor (NK-1R) alters adipose tissue responses to high-fat diet and insulin action. |
| 555 | 21467195 | Peripheral administration of a specific neurokinin-1 receptor (NK-1R) antagonist to mice leads to reduced weight gain and circulating levels of insulin and leptin after high-fat diet (HFD). |
| 556 | 21467195 | Here, we assessed the contribution of substance P (SP) and NK-1R in diet-induced obesity using NK-1R deficient [knockout (KO)] mice and extended our previous findings to show the effects of SP-NK-1R interactions on adipose tissue-associated insulin signaling and glucose metabolic responses. |
| 557 | 21467195 | Compared with WT, NK-1 KO mice show reduced weight gain and circulating levels of leptin and insulin in response to HFD. |
| 558 | 21467195 | Adiponectin receptor mRNA levels are higher in mesenteric fat and liver in NK-1 KO animals compared with WT, after HFD. |
| 559 | 21467195 | Mesenteric fat from NK-1R KO mice fed with HFD has reduced stress-activated protein kinase/c-Jun N-terminal kinase and protein kinase C activation compared with WT mice. |
| 560 | 21467195 | Substance P (SP)-neurokinin-1 receptor (NK-1R) alters adipose tissue responses to high-fat diet and insulin action. |
| 561 | 21467195 | Peripheral administration of a specific neurokinin-1 receptor (NK-1R) antagonist to mice leads to reduced weight gain and circulating levels of insulin and leptin after high-fat diet (HFD). |
| 562 | 21467195 | Here, we assessed the contribution of substance P (SP) and NK-1R in diet-induced obesity using NK-1R deficient [knockout (KO)] mice and extended our previous findings to show the effects of SP-NK-1R interactions on adipose tissue-associated insulin signaling and glucose metabolic responses. |
| 563 | 21467195 | Compared with WT, NK-1 KO mice show reduced weight gain and circulating levels of leptin and insulin in response to HFD. |
| 564 | 21467195 | Adiponectin receptor mRNA levels are higher in mesenteric fat and liver in NK-1 KO animals compared with WT, after HFD. |
| 565 | 21467195 | Mesenteric fat from NK-1R KO mice fed with HFD has reduced stress-activated protein kinase/c-Jun N-terminal kinase and protein kinase C activation compared with WT mice. |
| 566 | 21467195 | Substance P (SP)-neurokinin-1 receptor (NK-1R) alters adipose tissue responses to high-fat diet and insulin action. |
| 567 | 21467195 | Peripheral administration of a specific neurokinin-1 receptor (NK-1R) antagonist to mice leads to reduced weight gain and circulating levels of insulin and leptin after high-fat diet (HFD). |
| 568 | 21467195 | Here, we assessed the contribution of substance P (SP) and NK-1R in diet-induced obesity using NK-1R deficient [knockout (KO)] mice and extended our previous findings to show the effects of SP-NK-1R interactions on adipose tissue-associated insulin signaling and glucose metabolic responses. |
| 569 | 21467195 | Compared with WT, NK-1 KO mice show reduced weight gain and circulating levels of leptin and insulin in response to HFD. |
| 570 | 21467195 | Adiponectin receptor mRNA levels are higher in mesenteric fat and liver in NK-1 KO animals compared with WT, after HFD. |
| 571 | 21467195 | Mesenteric fat from NK-1R KO mice fed with HFD has reduced stress-activated protein kinase/c-Jun N-terminal kinase and protein kinase C activation compared with WT mice. |
| 572 | 21872660 | Nerve growth factor/p38 signaling increases intraepidermal nerve fiber densities in painful neuropathy of type 2 diabetes. |
| 573 | 21872660 | Similarly, Trk A-positive peptidergic IENF, which also express substance P and calcitonin gene related peptide in db/db mice, were observed to be elevated from 1.5 to 2 fold over controls. |
| 574 | 22009727 | Role of substance P in the regulation of glucose metabolism via insulin signaling-associated pathways. |
| 575 | 22009727 | Substance P (SP), encoded by the tachykinin 1 (Tac1) gene, is the most potent tachykinin ligand for the high-affinity neurokinin-1 receptor (NK-1R). |
| 576 | 22009727 | We previously reported that NK-1R-deficient mice show less weight gain and reduced circulating levels of leptin and insulin in response to a high-fat diet (HFD) and demonstrated the presence of functional NK-1R in isolated human preadipocytes. |
| 577 | 22009727 | We show that although weight accumulation in response to HFD was similar between Tac1(-/-) mice and wild-type littermates, Tac1(-/-) mice demonstrated lower glucose and leptin and increased adiponectin blood levels and showed improved responses to insulin challenge after HFD. |
| 578 | 22009727 | SP stimulated phosphorylation of c-Jun N-terminal kinase, protein kinase C, mammalian target of rapamycin, and inhibitory serine insulin receptor substrate-1 phosphorylation in human preadipocytes in vitro. |
| 579 | 22009727 | Preincubation of human mesenteric preadipocytes with the protein kinase C pseudosubstrate inhibitor reduced insulin receptor substrate 1 phosphorylation in response to SP. |
| 580 | 22009727 | These novel SP effects on molecules that enhance insulin resistance at the adipocyte level may reflect an important role for this peptide in the pathophysiology of type 2 diabetes. |
| 581 | 22009727 | Role of substance P in the regulation of glucose metabolism via insulin signaling-associated pathways. |
| 582 | 22009727 | Substance P (SP), encoded by the tachykinin 1 (Tac1) gene, is the most potent tachykinin ligand for the high-affinity neurokinin-1 receptor (NK-1R). |
| 583 | 22009727 | We previously reported that NK-1R-deficient mice show less weight gain and reduced circulating levels of leptin and insulin in response to a high-fat diet (HFD) and demonstrated the presence of functional NK-1R in isolated human preadipocytes. |
| 584 | 22009727 | We show that although weight accumulation in response to HFD was similar between Tac1(-/-) mice and wild-type littermates, Tac1(-/-) mice demonstrated lower glucose and leptin and increased adiponectin blood levels and showed improved responses to insulin challenge after HFD. |
| 585 | 22009727 | SP stimulated phosphorylation of c-Jun N-terminal kinase, protein kinase C, mammalian target of rapamycin, and inhibitory serine insulin receptor substrate-1 phosphorylation in human preadipocytes in vitro. |
| 586 | 22009727 | Preincubation of human mesenteric preadipocytes with the protein kinase C pseudosubstrate inhibitor reduced insulin receptor substrate 1 phosphorylation in response to SP. |
| 587 | 22009727 | These novel SP effects on molecules that enhance insulin resistance at the adipocyte level may reflect an important role for this peptide in the pathophysiology of type 2 diabetes. |
| 588 | 22009727 | Role of substance P in the regulation of glucose metabolism via insulin signaling-associated pathways. |
| 589 | 22009727 | Substance P (SP), encoded by the tachykinin 1 (Tac1) gene, is the most potent tachykinin ligand for the high-affinity neurokinin-1 receptor (NK-1R). |
| 590 | 22009727 | We previously reported that NK-1R-deficient mice show less weight gain and reduced circulating levels of leptin and insulin in response to a high-fat diet (HFD) and demonstrated the presence of functional NK-1R in isolated human preadipocytes. |
| 591 | 22009727 | We show that although weight accumulation in response to HFD was similar between Tac1(-/-) mice and wild-type littermates, Tac1(-/-) mice demonstrated lower glucose and leptin and increased adiponectin blood levels and showed improved responses to insulin challenge after HFD. |
| 592 | 22009727 | SP stimulated phosphorylation of c-Jun N-terminal kinase, protein kinase C, mammalian target of rapamycin, and inhibitory serine insulin receptor substrate-1 phosphorylation in human preadipocytes in vitro. |
| 593 | 22009727 | Preincubation of human mesenteric preadipocytes with the protein kinase C pseudosubstrate inhibitor reduced insulin receptor substrate 1 phosphorylation in response to SP. |
| 594 | 22009727 | These novel SP effects on molecules that enhance insulin resistance at the adipocyte level may reflect an important role for this peptide in the pathophysiology of type 2 diabetes. |
| 595 | 22154324 | A decreased sensory neuropeptide (SNP) release such as that of substance P, somatostatin, and calcitonin gene-related peptide determined from organ fluid of tracheal preparations subjected to electrical field stimulation also occurred in diabetic animals. |
| 596 | 23735822 | As a metabolic disorder depression has been associated with obesity, diabetes, insulin sensitivity, neuropeptide Y, glucose regulation, poor glycemic control, glucagone-like peptide-1, cholezystokinin, ghrelin, leptin, the endocannabinoid system, insulin-like growth factor and gastrin-releasing peptide. |
| 597 | 23735822 | Additionally blood coagulation, fibrinolysis, D-dimers, plasminogen activator inhibitor-1 protein, platelet activation, VEGF, plasma nitric oxide and its synthase are changed in depressed patients. |
| 598 | 23735822 | As an endocrinological and stress disorder depression has been connected with the concentration of free T4, TSH, CRH, arginine vasopressin, corticotrophin, corticosteroid release and ACTH. |
| 599 | 23735822 | Depression as an inflammatory disorder is mediated by pro-inflammatory cytokines, interleukin-1, interleukin-6, TNF-alpha, soluble interleukin-2 receptors, interferon-alpha, interleukin 8, interleukin-10, hs-CRP, acute phase proteins, haptoglobin, toll like receptor 4, interleukin-1beta, mammalian target of rapamycin pathway, substance P, cyclooxygenase-2, prostaglandin-E2, lipid peroxidation levels and acid sphingomyelinase. |
| 600 | 23735822 | The neurodegenerative hypothesis of depression explains decreased hippocampal volumes in depressed patients and changes of neurotrophic support by BDNF, erythropoietin, GDNF, FGF-2, NT3, NGF and growth hormone. |
| 601 | 23735822 | Hence, GABA, AMPA, EAAT, NMDA- and metabotropic glutamate receptors (mGluR1 to mGluR8) have gained interest in depression recently. |