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Gene Information
Gene symbol: AGT
Gene name: angiotensinogen (serpin peptidase inhibitor, clade A, member 8)
HGNC ID: 333
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 21269661 | The aim of the study was to determine in a rat model of streptozotocin-induced diabetic nephropathy the expression of: WT-1 (for podocyte loss in the glomerulus), TGF-beta 1 (for tissue damage), caspase-3 and bax (for glomerular apoptosis) and the possible protective effects of an angiotensin II type 1 receptor blocker. |
| 2 | 21269661 | We conclude that the decrease in the number of podocytes is an early marker of diabetic nephropathy, AT1 receptor blocker has renoprotective effects on the regulation of renal hemodynamics and on the control of tissue damage by preventing podocyte loss, which leads to decrease of bax and caspase-3 expressions of apoptosis related proteins, and may prevent glomerular cell apoptosis via angiotensin II. |
| 3 | 21912849 | It has been shown that oxidized low-density lipoprotein (ox-LDL) activates renin-angiotensin system (RAS) and angiotensin II via its type 1 receptor activates ox-LDL receptor LOX-1. |
| 4 | 21816757 | In conclusion, in type 2 diabetes concomitant blockade of ANG II synthesis and ET-1 biological activity through an ET(A) receptor antagonist led to substantial albeit not complete renoprotection, almost due to the ACE inhibitor. |
| 5 | 4373570 | Long-lasting haemorrhagic hypotension (4.5 hr at 35 mmHg) leading to irreversible haemorrhagic shock, has been studied in normal dogs, in dogs treated with a bradykinin potentiating nonapeptide (BPP(9a)), which blocks the conversion of angiotensin I to angiotensin II, and in dogs with experimental chronic diabetes insipidus (DI dogs). |
| 6 | 954671 | In comparison to findings in normal Long-Evans rats, pressor responses to intraventricular perfusions of angiotensin II were reduced in rats heterozygous for hypothalamic diabetes insipidus and virtually absent in rats homozygous for the hypothalamic deficiency whether they were treated with vasopressin or not. |
| 7 | 203196 | The effect of blockade of central angiotensin II (AII) receptors and cholinergic receptors on thirst induced by water deprivation was studied in Sprague-Dawley rats and rats with hereditary hypothalamic diabetes insipidus (DI). |
| 8 | 45468 | Normal human plasma contains "inactive renin," whose ability to generate angiotensin I increases after exposure to pH 3.3. |
| 9 | 7027426 | The amount of isorenin as well as of angiotensin I and II in the pineal gland depends on the circadian rhythm, the sleep-wakefulness cycle, osmotic stimuli, stimulation of the sympathetic postganglionar fibres which innervate the pineal gland and it is increased in some diseases, as hereditary diabetes insipidus and spontaneous hypertension in rat. |
| 10 | 7040751 | Plasma renin activity (PRA) and plasma aldosterone (PA) were measured under conditions of bed rest and after administration of furosemide and/or angiotensin II to adult-onset diabetics and age-matched controls. |
| 11 | 7051007 | In this study, the effects of glucose and insulin on the contractile response of cloned homogeneous cultures of rat glomerular mesangial cells to angiotensin II were examined. |
| 12 | 7051007 | From these data, it appears that insulin may be required for the contractile response of mesangial cells to angiotensin II. |
| 13 | 6337508 | Brattleboro rats with congenital diabetes insipidus were less sensitive to vasopressin than the other animals, and neither angiotensin II nor isoproterenol induced any change. |
| 14 | 6331195 | On a normal salt intake, glomerular ANG II receptor density was reduced significantly in untreated diabetic rats (853 +/- 74 (SE) fmol/mg protein), compared with insulin-treated diabetic rats (1,185 +/- 118 fmol/mg) and normal controls (1,058 +/- 83 fmol/mg). |
| 15 | 4047977 | Treatment with the angiotensin II antagonist, sar1-leu8-angiotensin II, before intravenous administration of angiotensin II prevented metabolic stimulation of the subfornical organ and neural lobe. |
| 16 | 3908320 | Pressor responsiveness to angiotensin II also may sometimes be increased relative to plasma renin levels. |
| 17 | 2868056 | Both i.c.v. methoxamine (10 micrograms/kg) and phenylephrine (30 micrograms/kg) also increased plasma levels of arginine vasopressin (AVP) in LE rats from 2.6 +/- 0.4 (n = 9) to 22.4 +/- 3.5 (n = 6, P less than 0.01) and 37.0 +/- 4.0 pg/ml (n = 6, P less than 0.01), respectively, without affecting plasma renin activity (PRA) and plasma angiotensin II (ANG II) levels. |
| 18 | 3091164 | The influence of angiotensin II on kidney function in diabetic nephropathy was assessed by studying the effect of 12 weeks' monotherapy with captopril (25-50 mg twice a day) in 16 hypertensive insulin dependent diabetic patients with persistent albuminuria. |
| 19 | 3325392 | Since the angiotensin converting enzyme (ACE) is identical with kininase II, the reduction of its activity by an ACE-inhibitor such as captopril will not only decrease the concentration of angiotensin II but also elevate the levels of kinins. |
| 20 | 3284388 | Our observations suggest that the abnormally elevated glomerular blood flow and filtration rate of early IDDM can be corrected by a low-sodium diet via stimulation of endogenous ANG II. |
| 21 | 3292327 | Insulin significantly and dose dependently inhibited the vasoconstriction induced by NE (10(-8) M for the artery and 10(-7) M for the vein) at greater than or equal to 1.2 mU/ml for both the artery and vein and the vasoconstriction induced by ANG II (3 x 10(-10) M for the artery and 3 x 10(-9) M for the vein) at greater than or equal to 1.2 mU/ml for the artery and greater than or equal to 12 mU/ml for the vein. |
| 22 | 3054274 | We review available data on the activity of the renin-angiotensin system (RAS), responsiveness to angiotensin II (ANG II), ANG II receptor number, and effects of inhibition of the RAS by angiotensin I converting enzyme (ACE) inhibitors in patients with diabetes mellitus. |
| 23 | 2853753 | These results indicate that ACE inhibition interferes with the glomerular capillary permeability induced by angiotensin II. |
| 24 | 2493961 | The cardiovascular effects of bolus intravenous injections of vasopressin, angiotensin II and noradrenaline were studied in 6-hydroxydopamine pretreated, anaesthetized Brattleboro rats with hereditary diabetes insipidus and normal rats of the parent Long Evans strain. 2. |
| 25 | 2498395 | Angiotensin II inhibition of hepatic adenylate cyclase was not altered in either diabetic rat. |
| 26 | 2527703 | Plasma renin activity and plasma angiotensin II were lower in both groups of diabetic patients than in the normal control subjects (p less than 0.01). |
| 27 | 2531549 | Likewise, raising perfusate glucose levels to 400 mg/dl or adding insulin (180 microU/ml) to the perfusate failed to modify responses to ANG II. |
| 28 | 2575661 | The effect of angiotensin converting enzyme (ACE) inhibition on kidney function in diabetic nephropathy showed that the GFR is not dependent on angiotensin II (Ang II), and that ACE inhibition diminished albuminuria, probably by lowering glomerular hypertension. |
| 29 | 2693655 | Thus, inhibition of Ang II generation may explain why angiotensin converting enzyme (ACE) inhibitors may be effective in arresting or slowing the progression of renal failure in experimental animals and in man. |
| 30 | 2408249 | ACE-inhibitors exhibit their blood pressure-lowering activity not only via a reduction of angiotensin II but also via on increase of kinin levels. |
| 31 | 2188897 | Elevated serum angiotensin converting enzyme activity and plasma renin activity, expressed as generated angiotensin I, were unaffected by the lower dose of insulin, but were reduced by 26% and 40%, respectively at the higher dose. |
| 32 | 2146596 | We investigated with the deoxyglucose method whether atriopeptin III, an atrial natriuretic peptide (ANP), would prevent this enhanced glucose metabolism and interfere with the drinking response in the presence of ANG II. |
| 33 | 1850348 | We examined the effects of EGF on basal and angiotensin II (AII)-induced aldosterone synthesis in freshly isolated rat and cultured human adrenal glomerulosa cells. |
| 34 | 1815656 | In our model, the role of renin I (prorenin) is to generate localized high concentrations of angiotensin II, eg, in the afferent arteriole of the kidney and in other vital organs, causing regional dilation by rendering tissues insensitive (tachyphylactic) to the vasoconstrictor effect of circulating angiotensin II or by releasing vasodilator substances. |
| 35 | 1619503 | Insulin-induced hypokalaemia increases plasma renin and angiotensin II levels while decreasing the serum aldosterone concentration. |
| 36 | 1386818 | This study suggests that the low renin state in DM may be explained by the enhanced inhibitory effect of ANG II and the resistance to the secretogogue actions of insulin and IGF-I. |
| 37 | 1513111 | Whereas plasma renin activity rose in both the perindopril and triple therapy groups, it is likely that the effects on angiotensin II levels were opposite since perindopril but not triple therapy was associated with a significant reduction in plasma angiotensin converting enzyme activity. |
| 38 | 1457255 | This could be explained by the fact that ACE-inhibitors suppress the trophic effects of angiotensin II on the nephron, while calcium channel blockers might interfere with intracellular processes involved in cell hypertrophy that require the interaction of calcium ions. |
| 39 | 8458051 | Patients at greatest risk of declining renal function during therapy with ACE inhibitors are those in whom maintenance of renal function is dependent on angiotensin II. |
| 40 | 8476260 | Angiotensin converting enzyme transforms angiotensin I into angiotensin II and breaks down bradykinin into inactive products. |
| 41 | 8285177 | In particular, ACE inhibitors appear to protect the kidney more than would be expected from simply the lowering of blood pressure and decreasing of intraglomerular pressure, possibly because angiotensin II has both hemodynamic and direct effects on the glomerulus. |
| 42 | 8285177 | Part of these seemingly inconsistent observations may be due to (1) potential activity of tissue RASs, (2) increased sensitivity to angiotensin II in diabetes, or (3) an effect of ACE inhibition on other systems in addition to the RAS. |
| 43 | 8130360 | In this study, the tissue-specific regulation of renin and angiotensinogen mRNA levels and the abundance of glomerular angiotensin II receptors were examined in male Sprague-Dawley rats (160 to 240 g) made diabetic with streptozotocin. |
| 44 | 8130360 | Angiotensinogen mRNA levels were significantly lower in the livers and adrenals of diabetic rats in comparison to those in controls and insulin-treated diabetic rats, whereas angiotensinogen mRNA levels in the brain remained unaltered. |
| 45 | 8275971 | The 12-lipoxygenase (LO) pathway of arachidonic acid plays an important role in angiotensin II (AII)-mediated aldosterone synthesis. |
| 46 | 8282345 | These results suggest that 12-lipoxygenase activation plays a key role in Ang II-induced vascular smooth muscle cell hypertrophy. |
| 47 | 8141164 | Finally, insulin potentiates the effects of other agonists (eg, thromboxane A2, angiotensin II) on vascular contraction and cell growth. |
| 48 | 8206589 | It is possible that the reduced magnesium content of the high-fructose commercial diet used in some studies may play a role in these abnormalities because it is known that magnesium deficiency can produce insulin insensitivity and increased angiotensin II action in humans. |
| 49 | 7698201 | The cardiovascular effects of intravenous injections of vasopressin, angiotensin II and noradrenaline were studied in anaesthetized adult male Brattleboro rats with hereditary diabetes insipidus on lifelong treatment with the vasopressin V2 receptor agonist desamino-8D-arginine vasopressin in the drinking fluid, which restored fluid input and output to normal rat values. |
| 50 | 7769497 | In particular, ACE inhibitors have actions beyond blockade of angiotensin II formation, necessitating cautious interpretation of data from their use. |
| 51 | 7840166 | In the present studies, we have examined the acute and chronic effects of insulin on angiotensin II (ANG II)-induced aldosterone synthesis in cultured normal and adenomatous human adrenal glomerulosa cells. |
| 52 | 7840166 | Short-term insulin treatment (1.5 h) resulted in inhibition of ANG II-induced aldosterone synthesis. |
| 53 | 7533733 | Similarly, ANG II (10(-8) mol/l) inhibition of renin was significantly enhanced in diabetic rats (P < 0.001). |
| 54 | 7533733 | Insulin reversed the inhibitory effects of ANG II on renin in normal rats, but it blunted the effect of ANG II in diabetic rats. |
| 55 | 7787143 | Six weeks after the onset of insulin-treated streptozotocin diabetes (STZ) in Munich-Wistar rats, the effect of a low-sodium (LNa) and a low-salt (LNaCl) diet on renal function and on plasma and kidney tissue angiotensin II (AIIp, AIIk) was tested. |
| 56 | 7653525 | In the presence of ethanol, ANG II markedly increased phosphatidylethanol (PEt) formation, indicating activation of phospholipase D (PLD). |
| 57 | 8800600 | Treatment with angiotensin converting enzyme (ACE) inhibitors ameliorates human and experimental diabetic nephropathy, possibly as a result of changes in angiotensin II (AngII) and/or bradykinin concentrations. |
| 58 | 9095091 | Chronic insulin exposure increased by 70% to 90% the [Ca2+]i response to both angiotensin II and bradykinin in control subjects and normotensive non-insulin-dependent diabetic patients but not in hypertensive patients. |
| 59 | 9374757 | In this study, we examined the regulation of VEGF expression in vascular smooth muscle cells (VSMC) by hyperglycemia as well as by angiotensin II (ANG II). |
| 60 | 9374757 | We also examined whether the 12-lipoxygenase (12-LO) product 12-hydroxyeicosatetraenoic acid (12-HETE) can alter VEGF expression, since 12-LO products of arachidonic acid have angiogenic properties, and ANG II as well as high glucose (HG, 25 mM) can increase 12-LO activity and expression in VSMC. |
| 61 | 9400384 | The change in PKC epsilon distribution and in TnI phosphorylation in diabetic animals was completely prevented by rendering the animals euglycemic with insulin or by concomitant treatment with a specific angiotensin II type-1 receptor (AT1) antagonist. |
| 62 | 10977776 | Evidence suggests that intrarenal RASs within glomeruli and proximal tubules may be activated with hyperglycemia, leading to stimulation of local ANG II production, which may exert feedback inhibition of systemic renin release. |
| 63 | 10981145 | Although these perceptions suggest that drugs interfering with ANG II effects (ACE inhibitors, AT1 -receptor antagonist) may serve as antioxidants, preventing vascular and renal changes, the clinical studies are not so straightforward. |
| 64 | 11115412 | Together with the findings that both ACE inhibition and angiotensin II blockade improve resistance vessel function in this group, it is likely that at least some of the beneficial effect is mediated through the angiotensin II/type I receptor pathway. |
| 65 | 11230339 | The proline-rich tyrosine kinase 2 (Pyk2) and paxillin are 2 cytoskeleton-associated proteins involved in cell movement, phosphorylated by Ang II in other cell types, and abundantly expressed in monocytes. |
| 66 | 11230339 | Ang II (1 micromol/L) induced Pyk2 and paxillin phosphorylation in human THP-1 monocytes, peaking after 10 minutes for Pyk2 with a 6.7+/-0.9-fold induction and after 2 minutes for paxillin with a 3.2+/-0.4-fold induction. |
| 67 | 11230339 | This study demonstrates a novel proatherogenic action of Ang II on human monocytes by stimulating their migration, through an AT1-R-dependent process, involving signaling through Src, ERK 1/2, and p38. |
| 68 | 11230339 | Furthermore, the promigratory actions of Ang II in human monocytes are associated with the phosphorylation of 2 cytoskeleton-associated proteins, Pyk2 and paxillin. |
| 69 | 11260405 | The high correlation between the renal hemodynamic response to captopril and to candesartan indicates that reduced angiotensin II formation is the main mechanism of action of the ACE inhibitor. |
| 70 | 11289054 | In this study, we investigated the effect of angiotensin II (AII) on Ang1 and Ang2 expression in cultured bovine retinal endothelial cells (BRECs). |
| 71 | 11422735 | Faster progression to ESRD is associated with the ACE genotype when the total population with ESRD and with the AGT genotype when patients with glomerulonephritis are considered. |
| 72 | 11508272 | We studied the expression of nephrin in a hypertensive model of diabetic nephropathy and investigated the potential influence of angiotensin II blockade on nephrin gene and protein expression. |
| 73 | 11508272 | These changes in nephrin levels were completely prevented by angiotensin II antagonist treatment, suggesting a potential novel mechanism to explain the antiproteinuric effect of agents which interrupt the renin-angiotensin system. |
| 74 | 11508273 | Diabetic rats were either untreated or received the angiotensin converting enzyme inhibitor ramipril, or the angiotensin II type 1 receptor antagonist, valsartan. |
| 75 | 11711055 | However, the effect of angiotensin II type-1 (AT(1)) receptor antagonists on insulin resistance is still controversial. |
| 76 | 11855793 | We compared the efficacy of treatment protocols with an angiotensin converting enzyme (ACE) inhibitor alone (enalapril, 5 mg) or angiotensin II (ATII) receptor blocker (losartan, 50 mg) or both enalapril plus losartan in patients with microalbuminuria in a prospective, randomized clinical trial. |
| 77 | 11881122 | Mean (+/-SD) serum angiotensin-converting enzyme (ACE) activity and plasma angiotensin II(Ang II) levels at days 17-18 of pregnancy were greater in the untreated diabetic rats than in control pregnant rats (ACE: 163+/-18 vs. 111+/-21 nmol/ml/minute, p<0.001, Ang II: 115+/-45 vs. 43+/-10 pg/ml, p<0.005). |
| 78 | 11881122 | Increased serum ACE activity during pregnancy and postpartum in the untreated diabetic rat is associated with enhanced serum Ang II levels, which may contribute to increased protein excretion and renal hypertrophy. |
| 79 | 11935151 | Treatment with ACE-inhibitors attenuates retinal overexpression of VEGF-A in patients with proliferative diabetic retinopathy, probably by interference with a local effect of angiotensin II. |
| 80 | 11967010 | Both high glucose (HG) and angiotensin II (Ang II) causes glomerular mesangial cell (GMC) growth and increased synthesis of matrix proteins like collagen IV contributing to diabetic nephropathy. |
| 81 | 11967010 | We hypothesized that Ang II activation of the JAK/STAT pathway is altered by HG in GMC, and that this pathway might be linked to the Ang II-induced growth and overproduction of collagen IV in GMC in HG conditions. |
| 82 | 11967010 | The HG and Ang II induced growth and collagen IV synthesis studies were performed in GMC transfected with JAK2 antisense or JAK2 sense. |
| 83 | 11967010 | We found that Ang II-induced JAK2, STAT1, STAT3, STAT5A/B and SHP-2 phosphorylations were enhanced by HG, whereas that of SHP-1 was reduced. |
| 84 | 11967010 | Transfection of GMC with JAK2 antisense oligonucleotides blocked the Ang II-induced growth and collagen IV synthesis in both NG and HG conditions. |
| 85 | 11991216 | These findings indicate that perindopril but not losartan decreases PAI-1 in hypertensive type 2 diabetic patients, which suggests that the PAI-1 lowering effect is unrelated with AT, receptor blockade and could rather be due to the fact that the endothelial receptors that mediate PAI-1 expression in response to angiotensin II are not type 1 receptor subtypes. |
| 86 | 12660870 | Thus, visceral cells transfer and release fatty acids more extensively, have increased glucocorticoid and reduced thiazolidinedione responses, produce more angiotensinogen, interleukin-6 and plasminogen activator inhibitor-1, and secrete less leptin and adiponectin than SAT. |
| 87 | 12676168 | Whereas angiotensin II promotes adipocyte growth and preadipocyte recruitment, increased secretion of angiotensinogen from adipocytes also directly contributes to the close relationship between adipose-tissue mass and blood pressure in mice. |
| 88 | 12692747 | Since renin catalyses the first and rate-limiting step of the renin-angiotensin system (RAS) cascade, interruption of the generation of angiotensin II (Ang II) by renin inhibitors at this highly specific initial step of the cascade has long been a therapeutic goal. |
| 89 | 12692747 | Due to the lack of effective alternative enzyme pathways, blockade of Ang II production may be more effective with renin inhibition than with angiotensin-converting enzyme (ACE) inhibition. |
| 90 | 12817909 | Plasma noradrenaline (NA, pmol/L), adrenaline (A, pmol/L), plasma renin activity (PRA, angiotensin I, nmol/L/h) and aldosterone (ALD, pmol/L) were measured in the supine position (baseline) and after 2, 5, and 20 min O in 10 healthy subjects (C), 9 T2D patients without AN (D), 14 T2D patients with AN and without PH (DAN), and 7 T2D patients with AN and PH (DAN-PH). |
| 91 | 12826071 | In human adult kidney angiotensin II (AngII) effects are mediated by the AT1 receptor, while the functions of AT2 receptors are mostly unknown. |
| 92 | 12826071 | Since AngII regulates endothelial cell growth by AT1 and AT2 receptors, we analysed their functional aspects at different passages in human glomerular endothelial cells (GENC). |
| 93 | 12826071 | In fact, binding studies of different families of displacement curves using AngII, DUP753 (AT1 antagonist), and PD123177 (AT2 antagonist) showed the presence of AT1a and AT2 receptors at 4p-9p while in GENC 2p only the presence of AT2. |
| 94 | 12826071 | AngII regulates the mitogenic effect through AT1a receptors (in later cell passages 4p-15p) involving the release of PDGF-BB, while AT2 (in early cell passage 2p) showed a predominant negative growth control. |
| 95 | 12829650 | However, the observed deleterious hemodynamic responses to high glucose and Ang II and the insensitivity to ACE inhibition may, taken together, provide an explanation for the adverse renal outcomes in patients with type 1 diabetes and high N/D ratio. |
| 96 | 12941779 | We recently found that activation of janus kinase 2 (JAK2) is essential for the Ang II-induced proliferation of vascular smooth muscle cells (VSMCs) and that high glucose augments Ang II-induced proliferation of VSMCs by increasing signal transduction through activation of JAK2. |
| 97 | 14555183 | Thus, angiotensin II induces the phosphorylation of 4E-BP1 via the PI 3-kinase/mTOR pathway, but not via ERK or p70 S6 kinase. |
| 98 | 12876066 | We postulated that diabetes-induced transforming growth factor (TGF)-beta production contributes to impaired ANG II response of vascular smooth muscle cells in macrovessels and microvessels. |
| 99 | 15257162 | However, when compared with placebo, ACE inhibition by ramipril or by the ARB, candesartan, both decrease the incidence of new diabetes, raising the hypothesis that these agents actually prevent the changes leading to insulin resistance, possibly by lessening the adverse effects of angiotensin II on the endothelium. |
| 100 | 15280531 | NF-kappaB is activated in experimental models of renal injury, and in vitro studies also suggest that proteinuria and angiotensin II could be important NF-kappaB activators. |
| 101 | 15271787 | In this review, we discuss the hypothesis that the protein tyrosine phosphatase (PTPase), PTP-1B, plays a central role in Ang II-induced insulin resistance by inhibiting activation of the insulin receptor. |
| 102 | 15271787 | We hypothesize that Ang II-induced PTP-1B activation leads to dephosphorylation of the insulin receptor and that this signaling pathway underlies the maladaptive responses observed in diabetic vascular and renal tissue during type II diabetes. |
| 103 | 15353911 | The present study was thus designed to examine the effect of an angiotensin II type 1 (AT1) receptor antagonist, irbesartan on renal function, oxidative stress and nitric oxide (NO) release in streptozotocin (STZ)-induced diabetic rats. |
| 104 | 15494545 | Infusion of ANG II (50 ng x kg(-1) x min(-1)) increased mean arterial pressure by approximately 7 mmHg in all groups of mice and reduced SNGFR in WT and ACE 1/3 mice (to 30.9 +/- 2.8 and 31.9 +/- 2.5 nl x min(-1) x g KW(-1)) while increasing it in ACE 2/2 mice (to 55.3 +/- 5.3 nl x min(-1) x g KW(-1)) despite an increase in total renal vascular resistance. |
| 105 | 15699040 | Similarly, incubation of cultured cardiomyocytes with AngII increased CTGF mRNA expression by 2-fold, which was blocked by candesartan and a general PKC inhibitor, GF109203X. |
| 106 | 15699040 | Thus, AngII can regulate CTGF expression in cardiomyocytes through a PKC activation-mediated pathway in an isoform-selective manner both in physiological and diabetic states and may contribute to the development of cardiac fibrosis in diabetic cardiomyopathy. |
| 107 | 15837949 | Tumor necrosis factor-alpha (TNF-alpha), an inducer of angiotensinogen in hepatocytes, is elevated in hyperinsulinemic, obese individuals and may provide a link in mediating insulin upregulation of the RAS in adipose tissue. |
| 108 | 15837949 | Subcutaneous adipocytes were also treated with TNF-alpha (10 to 100 ng/mL) to examine the direct effect on angiotensinogen expression and angiotensin II secretion. |
| 109 | 15837949 | Insulin increased TNF-alpha secretion in a concentration-dependent manner (P<0.01), whereas RSG (10 nmol/L) significantly reduced the insulin-mediated rise in TNF-alpha (P<0.001), as well as angiotensin and angiotensin II. |
| 110 | 15840669 | Cultured mouse podocytes were treated with various doses of AngII for selected periods of time, with or without inhibitors of TGF-beta and VEGF signalling, SB-431542 and SU5416, respectively. |
| 111 | 15840669 | AngII >or=10(-10) M was found to stimulate the production of alpha3(IV) collagen significantly in as short a time as 3 h. |
| 112 | 15840669 | The expression of alpha3(IV) collagen was influenced by the TGF-beta system, but AngII did not increase the podocyte's production of TGF-beta1 ligand; rather, it increased the expression of the TGF-beta type II receptor and activated the TGF-beta signalling system through Smad2. |
| 113 | 15840669 | However, blockade of TGF-beta signalling with SB-431542 prevented AngII from stimulating alpha3(IV) collagen production. |
| 114 | 15840669 | Blockade of the endogenous VEGF activity by SU5416 prevented AngII-stimulated alpha3(IV) collagen production. |
| 115 | 15840669 | AngII stimulates the podocyte to produce alpha3(IV) collagen protein via mechanisms involving TGF-beta and VEGF signalling. |
| 116 | 15864528 | Plasma concentrations of adiponectin and adipose tissue levels of adiponectin mRNA were decreased in AngII-infused rats, and this effect was prevented by cotreatment with tempol or BH4. |
| 117 | 15864528 | Since antioxidants were observed to prevent the actions of AngII, and H2O2 on its own suppressed adiponectin expression, we conclude that adiponectin gene expression is negatively modulated by oxidative stress. |
| 118 | 15922295 | In db/db mice, oral administration of angiotensin II Type 1 receptor antagonist valsartan (5 mg/kg) for 4 weeks significantly attenuated the increased expression of gp91phox and p22phox together with inhibition of oxidative stress and partially restored decreased insulin contents in islets. |
| 119 | 15934924 | As increasing the levels of ACE by approximately 50% in this polymorphism is only calculated to increase the levels of angiotensin II by < 5%, whereas the levels of bradykinin will decrease by 20%, bradykinin may be nephroprotective. |
| 120 | 15952590 | The plasma Ang II level was assayed with 125I-Ang II radioimmunoassay, and the expression of AT1 in blood vessel and kidney was analyzed with immunohistochemical technique. |
| 121 | 15952590 | The plasma Ang II levels and the expression of AT1 in type 2 diabetic and high fat diet rats increased. |
| 122 | 15952590 | Enalapril was shown to decrease the plasma Ang II level and downregulate the expression of AT1 in blood vessels and kidneys in type 2 diabetic rats. |
| 123 | 15939809 | To identify new antidiabetic mechanisms of ARBs, we studied the regulation of adiponectin by angiotensin II (Ang II) and different ARBs in murine 3T3-L1 adipocytes and obese Zucker rats. |
| 124 | 15939809 | Adiponectin protein expression was markedly stimulated by Ang II (5 nmol/L), which was inhibited by blockade of the AT2R, and further enhanced by the ARB irbesartan. |
| 125 | 15939809 | Irbesartan-mediated adiponectin upregulation started beyond the concentrations needed for AT1R blockade and was also present in the absence of Ang II, implicating an AT1R-independent mechanism of action. |
| 126 | 15998260 | Recently, we reported that lysophosphatidylcholine, a major bioactive product of oxidized low-density lipoprotein, and angiotensin II, a vasoactive hormone and a potent inducer of reactive oxygen species (ROS), negatively regulate insulin signaling in vascular smooth muscle cells (VSMCs). |
| 127 | 16007228 | Most of the negative cardiovascular actions of angiotensin II are mediated through AT1 receptors, whereas the AT2 receptors mediate largely beneficial effects. |
| 128 | 15998704 | The aim of the present study was 2-fold: (1) to characterize the cardiovascular phenotype of p66Shc knockout mice (p66Shc(-/-)), and (2) to test the novel hypothesis that disrupting the p66Shc might protect the heart from the damaging action of elevated Ang II levels. |
| 129 | 15998704 | In p66Shc(+/+), infusion of a sub-pressor dose of Ang II (300 nmol/kg body weight [BW] daily for 28 days) caused left ventricular hypertrophy and apoptotic death of cardiomyocytes and endothelial cells. |
| 130 | 15998704 | Consistently, in vitro experiments showed that Ang II causes apoptotic death of cardiomyocytes isolated from p66Shc(+/+) hearts to a greater extent as compared with p66Shc(-/-) cardiomyocytes. |
| 131 | 15998704 | In perspective, p66Shc inhibition may be envisioned as a novel way to prevent the deleterious effects of Ang II on the heart. |
| 132 | 15859946 | We questioned whether PCs express a functional phagocyte-type NAD(P)H oxidase, and examined the role of angiotensin II and high glucose on the activity of the oxidase complex and expression of the essential subunit p22(phox). |
| 133 | 16084009 | Contractile responses to ANG II was significantly inhibited by type 1 ANG II receptor (AT1) antagonist but not by type 2 ANG II receptor (AT2) antagonist in both groups. |
| 134 | 16503870 | In this review the effect of inhibiting the renin-angiotensin system with angiotensin converting enzyme inhibition and a comparison to angiotensin II receptor antagonism is discussed, with the results of clinical trails reflecting the more recently discovered, non-haemodynamic, proatherogenic actions of angiotensin II. |
| 135 | 16614731 | Through the inhibition of ACE and ECE, it blocks the conversion of angiotensin I (AI) and big endothelin-1 (big ET-1) into the two most potent peptidic vasoconstrictors, angiotensin II (AII) and ET-1, respectively. |
| 136 | 16146787 | We hypothesize that chronically elevated intrarenal angiotensin II (ANG II) down-regulates nephrin, a key slit-pore protein and up-regulates fibrogenic molecule transforming growth factor (TGFbeta1) and thus result in progression of nephropathy in type 2 diabetes. |
| 137 | 16146787 | Captopril treatment prevented increase in intrarenal ANG II, and reversed expression of nephrin, TGFbeta1, collagen and fibronectin. |
| 138 | 16310163 | Both glucose and angiotensin II (Ang II) upregulate thrombospondin-1 (TSP1), a major activator of latent TGF-beta, and stimulate increased TGF-beta activity. |
| 139 | 16310163 | In this paper, we examined whether Ang II similarly upregulates TSP1 production and TSP1-dependent TGF-beta activation alone or in combination with high glucose concentrations. |
| 140 | 16310163 | Ang II and high glucose stimulated increases in TSP1 protein levels in the conditioned media of both rat cardiac fibroblasts (RCFs) and rat mesangial cells (RMCs). |
| 141 | 16310163 | Meanwhile, Ang II stimulated increases in both TGF-beta activity and protein by RMCs, whereas, RCFs responded to both Ang II and high glucose with increased TGF-beta activity in the absence of altered TGF-beta protein levels. |
| 142 | 16310163 | Moreover, Ang II induction of TSP1 and increased TGF-beta activity were blocked by losartan, an antagonist of the Ang II type 1 (AT1) receptor. |
| 143 | 16310163 | The increase in TSP1 expression leads to increased TGF-beta activity upon Ang II and/or glucose treatment, since peptide antagonists of TSP1-mediated TGF-beta activation blocked Ang II and glucose-induced TGF-beta activation. |
| 144 | 16340660 | Moreover, at least one other angiotensin-converting enzyme homologue (ACE2) plays a significant role in the regulation of heart and kidney function, and as it generates angiotensin 1-7 from angiotensin I, it is proposed to counteract the detrimental effects associated with the activation of the classic renin-angiotensin system. |
| 145 | 16344371 | We evaluated the effects of the PPAR-gamma activator rosiglitazone on Ang II signaling in aorta and mesenteric arteries. |
| 146 | 16344371 | Akt activity was increased by Ang II and returned to basal levels under rosiglitazone in both vascular beds. |
| 147 | 16398568 | Telmisartan (Micardis, Pritor), a highly selective angiotensin II (AII) type 1 (AT1) receptor antagonist, is approved for the treatment of hypertension, either as monotherapy or in combination with other antihypertensive agents. |
| 148 | 16389635 | At the extracellular level, the angiotensin-converting enzyme controls angiotensin II synthesis but also interferes with insulin signaling through the proper regulation of angiotensin II and through the accumulation of bradykinin. |
| 149 | 16389635 | At an early intracellular level, angiotensin II, acting through JAK-2/IRS-1/PI3-kinase, JNK and ERK, may induce the serine phosphorylation and inhibition of key elements of the insulin-signaling pathway. |
| 150 | 16389635 | Finally, by inducing the expression of the regulatory protein SOCS-3, angiotensin II may impose a late control on the insulin signal. |
| 151 | 16449288 | We investigated the effect of in vivo treatment by rosiglitazone on angiotensin II (A-II) stimulated manifestations of inflammation in cultured renal mesangial cells, such as proliferation, apoptosis, TGF-beta1 production and nuclear factor kappaB (NF-kappaB) activation, in the situation of pregnancies, complicated or not with diabetes. |
| 152 | 16556868 | Second, Ang II was also able to activate the late Smad2/3 signaling pathway at 24 hours, which was TGF-beta dependent because it was blocked by the anti-TGF-beta antibody and DN-TbetaRII. |
| 153 | 16556868 | Finally, activation of Smad3 but not Smad2 was a key and necessary mechanism of Ang II-induced vascular fibrosis because Ang II induced Smad3/4 promoter activities and collagen matrix expression was abolished in VSMCs null for Smad3 but not Smad2. |
| 154 | 16556868 | Thus, we concluded that Ang II induces vascular fibrosis via both TGF-beta-dependent and ERK1/2 MAPK-dependent Smad signaling pathways. |
| 155 | 16556868 | Activation of Smad3 but not Smad2 is a key mechanism by which Ang II mediates arteriosclerosis. |
| 156 | 16141358 | Angiotensin II (Ang II) activates a wide spectrum of signaling responses via the AT1 receptor (AT1R) that mediate its physiological control of blood pressure, thirst, and sodium balance and its diverse pathological actions in cardiovascular, renal, and other cell types. |
| 157 | 16141358 | Ang II-induced AT1R activation via Gq/11 stimulates phospholipases A2, C, and D, and activates inositol trisphosphate/Ca2+ signaling, protein kinase C isoforms, and MAPKs, as well as several tyrosine kinases (Pyk2, Src, Tyk2, FAK), scaffold proteins (G protein-coupled receptor kinase-interacting protein 1, p130Cas, paxillin, vinculin), receptor tyrosine kinases, and the nuclear factor-kappaB pathway. |
| 158 | 16141358 | Many of the deleterious actions of AT1R activation are initiated by locally generated, rather than circulating, Ang II and are concomitant with the harmful effects of aldosterone in the cardiovascular system. |
| 159 | 16775600 | This article reviews the HO system and the extent to which it influences the function of the healthy kidney; it summarizes conditions and stimuli that elicit HO-1 in the kidney; and it explores the significance of renal expression of HO-1 as induced by ischemia, nephrotoxins, nephritides, transplantation, angiotensin II, and experimental diabetes. |
| 160 | 16872231 | Promising additional strategies include ACE inhibitors and angiotensin II type 1 receptor antagonists because of their effectiveness and good tolerability in patients with migraine, particularly in those with hypertension. |
| 161 | 16728425 | In cultured cells, both high glucose and Ang-II induced significant increases in TGF-beta1, TIMP-2, and in collagen synthesis, and significant decreases in MMP-2 gene expression and activity, and thus disrupted the balance between MMP-2 and TIMP-2. |
| 162 | 16728425 | Moreover, treatment with a selective angiotensin type 1 (AT1) receptor antagonist significantly inhibited Ang-II mediated changes in TGF-beta1, MMP-2, TIMP-2, and in collagen production, suggesting the role of the AT1 receptor. |
| 163 | 16728425 | The addition of exogenous TGF-beta1 produced an effect similar to those of high glucose and Ang-II. |
| 164 | 16728425 | Furthermore, the inhibition of TGF-beta1 protein prevented Ang-II-induced MMP-2 and TIMP-2 alterations, suggesting the involvement of a TGF-beta1 pathway. |
| 165 | 16728425 | High glucose or Ang-II treatment induce alterations in MMP-2 and TIMP-2 balance, which favour TIMP-2 over-activity. |
| 166 | 16728425 | Moreover, Ang-II-mediated changes in the productions of MMP-2 and TIMP-2 occur via AT1 receptors and a TGF-beta1-dependent mechanism. |
| 167 | 16767106 | Here we examined the effect of Ang II on the expression of Smad1 and mesangial matrix expansion in streptozotocin (STZ)-induced diabetic rats in vivo, using Ang II type 1 receptor blocker, olmesartan. |
| 168 | 16767106 | Taken together, these results indicate that Ang II can regulate the development of mesangial matrix expansion in the early phase of diabetic nephropathy through Src and Smad1. |
| 169 | 16987014 | NADPH oxidase activity is upregulated by prolonged infusion of angiotensin II (Ang II) or a high salt diet. |
| 170 | 16987014 | Indeed, recent studies with small interference RNAs (siRNAs) targeted to p22( phox ) implicate p22( phox ) in Ang II-induced activation of renal NADPH oxidase and the development of oxidative stress and hypertension, while studies with apocynin implicate activation of p47( phox ) in the development of nephropathy in a rat model of type 1 diabetes mellitus (DM). |
| 171 | 16837815 | High glucose and angiotensin II (Ang II) can activate protein kinase C (PKC) in diabetes mellitus. |
| 172 | 16855220 | On the contrary, the contractile response involving the phosphorylation of MYPT1 and MLC20, and increased ROKalpha activity stimulated by ANG II were all abolished by overexpressing active Akt. |
| 173 | 16954165 | In the analysis of gene-gene interaction, these effects of the AGT 235T homozygotes on HRV sympathetic index were more apparent in the presence of the ACE D allele. |
| 174 | 16954165 | These data suggest that the AGT M235T polymorphism is associated with sympathetic predominance at rest, and AT1R 1166C allele carriers have potentially increased sympathetic response. |
| 175 | 17004092 | Since a crosstalk between AGE and angiotensin II (Ang II) has been proposed in the pathogenesis of accelerated atherosclerosis in diabetes, we examined here whether and how telmisartan, a unique Ang II type 1 receptor blocker (ARB) with peroxisome proliferator-activated receptor-gamma (PPAR-gamma)-modulating activity, could inhibit AGE-induced CRP expression in a human hepatoma cell line, Hep3B cells. |
| 176 | 17083070 | Firstly, angiotensin II (Ang II) and aldosterone produce similar biological effects and Ang II withdrawal has been shown to benefit patients with angina; aldosterone blockade may therefore follow in the footsteps of ACE inhibitors, as it did in heart failure, and produce benefits in vascular patients without heart failure. |
| 177 | 17074304 | In growth-arrested VSMCs, rosiglitazone attenuated the proliferation and apoptosis, increased PPAR-gamma production and activation, and reduced CTGF and ECM production in response to Ang II in a dose-dependent fashion. |
| 178 | 17342175 | Our results show that the overexpression of catalase prevents the stimulation of ROS and angiotensinogen mRNA in tubules owing to elevated glucose or angiotensin II in vitro. |
| 179 | 17359956 | Apelin treatment strikingly reversed the altered aortic vascular responsiveness to Ang II and acetylcholine in db/db mice, both of which were abolished by the eNOS inhibitor NG-nitro-L-arginine methyl ester. |
| 180 | 17359956 | Apelin treatment modulates the abnormal aortic vascular tone in response to Ang II and acetylcholine by potentiating phosphorylation of Akt and eNOS in diabetic mice, suggesting that the apelin-APJ system might be an important regulator of vascular function in diabetes. |
| 181 | 17487250 | This review discusses some of the studies that highlight the importance of IGF-1R transactivation in mediating Ang II- and H2O2-induced mitogen-activated protein kinase and protein kinase B signaling pathways. |
| 182 | 17493472 | Cox regression analyses using age, gender, hypertension, diabetes, ejection fraction, left atrial diameter, use of antiarrhythmic drugs, angiotensin-converting enzyme inhibitors or angiotensin II antagonists, and statins, and CRP quartiles as covariates showed that only CRP was independently associated with AF recurrence during follow-up (hazard ratio 4.98, 95% confidence interval 1.75 to 14.26, p = 0.003). |
| 183 | 17518348 | Angiotensin enzyme inhibitors (ACEi) and angiotensin-II receptor antagonists (ARBs) reduce proteinuria and retard the progression of renal failure in patients with IDDM and diabetic rats. |
| 184 | 17307998 | Our work suggests that ANG II, formed by the enzymatic activity of ACE and chymase, plays an important role in inducing postischemic LR and LA, effects that involve the engagement of both AT(1) and AT(2) receptors and may be mediated by CGRP and NADPH oxidase. |
| 185 | 17533199 | Angiotensin II, acting through its angiotensin type 1 receptor, inhibits the actions of insulin in the vasculature which may lead to deleterious effects such as vascular inflammation, remodeling, endothelial dysfunction, and insulin resistance. |
| 186 | 17533199 | To explore the impact of angiotensin II on insulin signaling, NADPH oxidase-derived reactive oxygen species formation, vascular inflammation, apoptosis, and remodeling, we used transgenic TG(mRen2)27 (Ren2) rats, which harbor the mouse renin transgene and exhibits elevated tissue angiotensin II levels. |
| 187 | 17600118 | Although kidney levels of angiotensin (Ang) II were not increased in the diabetic mice, treatment with an Ang II receptor blocker reduced urinary albumin excretion rate in Ace2(-/y)Ins2(WT/C96Y) mice, suggesting that acceleration of kidney injury in these mice is Ang II-mediated. |
| 188 | 17653207 | Angiotensin II (ANG II) plays an important role in its development through epidermal growth factor receptor (EGFR) transactivation. |
| 189 | 17653209 | As a result, many investigations have demonstrated that the diabetic milieu per se, hemodynamic changes, and local growth factors such as transforming growth factor-beta and angiotensin II, which are considered mediators in the pathogenesis of diabetic nephropathy, induce directly and/or indirectly hypertrophy, apoptosis, and structural changes, and increase type IV collagen synthesis in podocytes. |
| 190 | 17596525 | The renoprotection conferred by deletion of B2KR was associated with increased renal expression of B(1)-kinin and angiotensin II AT(2) receptors and decreased expression of connective tissue growth factor. |
| 191 | 17699555 | Patch-clamp experiments showed that ANG II-stimulated membrane currents in MCs were significantly attenuated or enhanced by knockdown or overexpression of TRPC6, respectively. |
| 192 | 17699555 | Fura-2 fluorescence measurements revealed that the ANG II-induced Ca(2+) influxes were markedly inhibited in MCs with TRPC6 knockdown, reminiscent of the impaired Ca(2+) entry in response to ANG II in high glucose-treated MCs. |
| 193 | 17897017 | Angiotensin converting enzyme (ACE) is a key enzyme in the renin angiotensin system (RAS) and converts angiotensin (Ang) I to the vasoconstrictor Ang II, which is thought to be responsible for most of the physiological and pathophysiological effects of the RAS. |
| 194 | 17897017 | This classical view of the RAS was challenged with the discovery of the enzyme, ACE2 which both degrades Ang II and leads to formation of the vasodilatory and anti-proliferative peptide, Ang 1-7. |
| 195 | 17560613 | Since the crosstalk between the AGEs-RAGE and the renin-angiotensin system has also been proposed in the pathogenesis of PDR, we investigated here whether olmesartan, an angiotensin II type 1 receptor blocker, inhibited the AGEs-elicited angiogenesis in vitro by suppressing the NF-kappaB-mediated RAGE expression. |
| 196 | 18316001 | Evidence indicates that CRP has a direct proatherogenic effect through up-regulation of angiotensin II type 1 receptors and through the stimulation of other proinflammatory factors. |
| 197 | 18326228 | To study prevalence and clinical implications of paradoxical rise of angiotensin II (AII) level in blood plasma in long-term therapy with ACE inhibitors in patients with type 2 diabetes mellitus (DM-2) and diabetic nephropathy (DN). |
| 198 | 18223023 | While ACE promotes angiotensin (Ang) II formation from Ang I, ACE2 degrades Ang II and Ang I. |
| 199 | 18305124 | Regarding potential mediators of these differences, offspring of diabetic mice had increased expression of intrarenal angiotensinogen and renin mRNA, upregulation of NF-kappaB isoforms p50 and p65, and activation of the NF-kappaB pathway. |
| 200 | 18469441 | The effects of hyperglycemia, a condition observed in diabetes, on angiotensin II type 1 receptor (AT1R) expression and beta-cell secretory function have yet to be explored. |
| 201 | 18511847 | Cardiomyocyte-specific PPARgamma(-/-) mice (cPPARgamma(-/-)) developed spontaneous cardiac hypertrophy with increased ventricular osteopontin expression and macrophage content, which were exacerbated by AngII infusion. |
| 202 | 18614617 | In these rats, angiotensin II caused significantly higher accumulation of inositol trisphosphate (IP3) and phospholipase C (PLC) activation which was sensitive to blockade by AT1 but not to AT2 antagonist. |
| 203 | 18619489 | The cardiac action of Ang II is influenced by the activity of different isoforms of ACE leading to different amounts of Ang II by comparison with other angiotensinogen-derived peptides. |
| 204 | 18619489 | The intracellular effects of Ang II are influenced by nitric oxide (NO)/cGMP-dependent cross talk and are mediated by the release of autocrine factors, such as transforming growth factor (TGF)-beta1 and interleukin (IL)-6. |
| 205 | 18792876 | In the first part of this paper, we review clinical studies to support the concept that angiotensin II type 1 receptor blockers (ARBs) could prevent the development of AF in insulin resistant patients and discuss the possible underlying mechanisms. |
| 206 | 18804122 | Excessive stimulation by the octapeptide angiotensin II contributes to a range of cardiovascular pathologies and diseases via angiotensin type 1 receptor (AT1R) activation. |
| 207 | 18818245 | NKA alpha-1 Ser23 phosphorylation was higher both in D7 and ANGII-treated rats in the non-cytoskeletal fraction, while no signal was detected in the cytoskeletal fraction. |
| 208 | 18829990 | In the present study, we determined whether hyperglycemia activates the cardiac intracellular renin-Ang system (RAS) in vivo and whether ARBs, ACE, or renin inhibitors block synthesis and effects of intracellular Ang II (iAng II). |
| 209 | 18949565 | We also aimed to investigate the post-effects of angiotensin II blockage treatment on clusterin expression and to compare these with apoptosis. |
| 210 | 19021774 | The enhancement of angiotensin II cleavage by R514Q ACE2 was a result of a 2.5-fold increase in V(max) compared with the wild-type. |
| 211 | 19029977 | These results suggest that the combination of high plasma angiotensin II and insulin with a diabetic state induced enhancement of endothelin-1-induced vasoconstriction, ET(A) receptor expression and ERK expression/activity in the aorta. |
| 212 | 19034303 | Angiotensin converting enzyme (ACE) generates angiotensin II from angiotensin I, which plays a critical role in the pathophysiology of diabetic nephropathy. |
| 213 | 19034303 | However, ACE2 generates angiotensin 1-7, which may protect the kidney by attenuating the effects of angiotensin II, since deletion of the Ace2 gene leads to glomerulosclerosis in mice, and pharmacologic inhibition of ACE2 exacerbates experimental diabetic nephropathy. |
| 214 | 18676994 | Proteins related to cell growth (CYR61, protein NOV, and clusterin) were increased, whereas growth arrest-specific 6 (GAS6) and growth/differentiation factor 6 were decreased by Ang II stimulation. |
| 215 | 19124424 | There may be a therapeutic rationale to prefer ARBs over ACE-Is in well-selected patients with congestive heart failure (CHF) because a considerable amount of angiotensin II (Ang II) is produced independent of angiotensin-conversion-enzyme (ACE) in the failing heart and is therapeutically unaffected by ACE-I treatment. |
| 216 | 19183745 | The renin-angiotensin system (RAS) can be inhibited through inhibition of angiotensin I (Ang I) generation from angiotensinogen by direct renin inhibitors, inhibition of angiotensin II (Ang II) generation from angiotensin I by angiotensin-converting enzyme inhibitors and finally by direct inhibition of the action of Ang II receptor level. |
| 217 | 19081082 | Ang II activates NAD(P)H oxidase in several tissues with important function in the control of insulin secretion. |
| 218 | 19081082 | We found that ANGII-induced superoxide generation via NAD(P)H oxidase activation and increased protein and mRNA levels of NAD(P)H oxidase subunits (p47(PHOX) and gp91(PHOX)). |
| 219 | 19107135 | In this study, we showed that blockade of Ang II attenuates vascular endothelial growth factor (VEGF)-mediated BRB breakdown in DR. |
| 220 | 19107135 | Ang II induced VEGF expression in retinal endothelial cells accompanied by loss of tight junction proteins. |
| 221 | 19107135 | However, the blockade of Ang II by perindopril, an angiotensin converting enzyme (ACE) inhibitor, inhibited upregulation of VEGF, and prevented the loss of tight junction proteins. |
| 222 | 19114589 | Inhibitors of the angiotensin-converting enzyme (ACE) decrease angiotensin II production and activate an intracellular signaling cascade that affects gene expression in endothelial cells. |
| 223 | 19193728 | EMSA and ChIP assays demonstrated increased p65/p50 binding to a NF-kappaB binding site at -1734 in the AGT gene promoter upon high glucose stimulation, and the binding was disrupted by 1,25(OH)(2)D(3) treatment. |
| 224 | 19193728 | These data indicate that 1,25(OH)(2)D(3) suppresses hyperglycemia-induced AGT expression by blocking NF-kappaB-mediated pathway. |
| 225 | 19196886 | Ramipril decreased systolic and diastolic blood pressure, ACE activity, and angiotensin II and increased plasma renin activity. |
| 226 | 19251743 | In addition, angiotensin (Ang) II is able to induce insulin resistance and an inflammatory state through Ang II receptor type 1 (AT1R). |
| 227 | 19375596 | Plasma Ang II is associated with body weight, decreases during weight loss, and is associated with markers of insulin resistance in obese subjects with T2D. |
| 228 | 19379059 | ACE inhibition by perindopril has two main effects: it inhibits the angiotensin II formation and potentiates bradykinin. |
| 229 | 19436651 | AT1R blockade may therefore be valuable treatment for early INSR as antagonism of AT1 receptors would allow angiotensin II to act unopposed at AT2 receptors. |
| 230 | 19445841 | These results suggest that Ang II can take part in induction of oxidative stress in diabetic rat heart and that blockage of its activity by AT1 receptor blocker is potentially protective against diabetes-induced cellular damage. |
| 231 | 19665690 | Because angiotensin II (Ang II) inhibits sensory neuron activation by interacting with Ang II type 1 (AT(1)) receptors, it is possible that AT(1) receptor blockers (ARBs) increase IGF-I production in SHRs. |
| 232 | 19679549 | Treatment of human pancreatic cancer cells (PANC-1, MIAPaCa-2, and BxPC-3) with insulin (10 ng/mL) for 5 minutes markedly enhanced the increase in intracellular [Ca(2+)] induced by GPCR agonists (e.g., neurotensin, bradykinin, and angiotensin II). |
| 233 | 19583814 | Infusion of angiotensin II (Ang II) also significantly induced ER stress and apoptosis in the hearts of WT, but not in MT-TG mice. |
| 234 | 19641301 | (Pro)renin receptor may contribute to the generation of arterial angiotensin II in kidney failure patients. |
| 235 | 19861503 | The results showed that D-glucose treatment up-regulates prorenin, renin, angiotensin II, PRR, IL-1beta, and COX-2 mRNA and protein expression and increases phosphorylation of ERK1/2, c-Jun N-terminal kinase, c-Jun, and nuclear factor-kappaB (NF-kappaB) p65 (serine 276,468 and 536), respectively. |
| 236 | 19861503 | PRR small interfering RNA attenuated PRR, IL-1beta, and COX-2 mRNA and protein expressions and significantly decreased angiotensin II production and phosphorylation of ERK1/2 and NF-kappaB p65 associated with high glucose exposure. |
| 237 | 19929182 | In people with screen-detected type 2 diabetes in primary care, (1) to assess adherence to guidelines, recommending consultation with the GP every three months and treatment initiation with an ACE inhibitor or an angiotensin-II receptor antagonist when systolic BP was > 120 mmHg and/or diastolic BP was > 80 mmHg, and (2) to identify predictors for adherence. |
| 238 | 19940327 | Adipose tissue produces multiple cytokines(TNF-alpha, IL-6, PAI-1, CRP, angiotensinogen, leptin, adiponectin, visfatin, apelin, resistin)which decrease insulin sensitivity and induce inflammatory processes, endothelial dysfunction,and atherosclerosis. |
| 239 | 19942847 | Three substance classes that block RAS-activation are currently available, angiotensin converting enzyme (ACE) inhibitors, angiotensin II type 1 receptor blockade (ARB) and renin inhibitors. |
| 240 | 19884815 | Thus, in patients, an increase in urinary angiotensinogen levels is observed, and this increase is precedent to an increase in urinary albumin levels, suggesting that urinary angiotensinogen may function as an early marker of diabetic nephropathy. |
| 241 | 20029537 | Since vasoactive peptides elicit their responses through generation of reactive oxygen species, including H2O2, we investigated whether IGF-1R transactivation plays a similar role in ET-1- and Ang II-induced PKB phosphorylation and hypertrophic responses in vascular smooth muscle cells (VSMC). |
| 242 | 20029537 | AG1024, a specific inhibitor of IGF-1R protein tyrosine kinase (PTK), attenuated both ET-1- and Ang II-induced PKB phosphorylation in a dose-dependent manner. |
| 243 | 20029537 | ET-1 and Ang II treatment also induced the phosphorylation of tyrosine residues in the autophosphorylation sites of IGF-1R, which were blocked by AG1024. |
| 244 | 20029537 | In addition, both ET-1 and Ang II evoked tyrosine phosphorylation of c-Src, a nonreceptor PTK, whereas pharmacological inhibition of c-Src PTK activity by PP2, a specific inhibitor of Src-family tyrosine kinase, significantly reduced PKB phosphorylation as well as tyrosine phosphorylation of IGF-1R induced by the 2 vasoactive peptides. |
| 245 | 20029537 | In conclusion, these data suggest that IGF-1R PTK and c-Src PTK play a critical role in mediating PKB phosphorylation as well as hypertrophic and proliferative responses induced by ET-1 and Ang II in A10 VSMC. |
| 246 | 19906946 | Indeed, podocyte stretching induced both angiotensin II secretion and AT(1) receptor overexpression, podocyte exposure to angiotensin II reduced nephrin protein expression, and both the AT-1 receptor antagonist candesartan and a specific anti-angiotensin II antibody completely abolished stretch-induced nephrin downregulation. |
| 247 | 20479236 | The ACE polymorphism does not significantly affect blood pressure or angiotensin II levels, suggesting that the kallikrein-kinin system partly mediates the effects of the polymorphism. |
| 248 | 20020514 | The results suggest that the PJ extract could prevent the development of high blood pressure induced by Ang II in diabetic rats probably by combating the oxidative stress induced by diabetes and Ang II and by inhibiting ACE activity. |
| 249 | 20671240 | Similarly, selective inhibition of ACE2 with MLN-4760 also resulted in a proinflammatory phenotype with a physiological response similar to that observed with exogenous Ang II (10(-7) mol/L). |
| 250 | 18413493 | Ang II type 1 receptor blockade with Olmesartan reduced CD renin to control levels but significantly increased juxtaglomerular renin. |
| 251 | 18931023 | Ovariectomized Wistar rats consuming a high-sodium diet received one of four treatments (n=7 per group): group 1, placebo pellets; group 2, E(2) (0 x 5 mg/pellet, 21-day release); group 3, NOS inhibitor, N(omega)-nitro-L-arginine-methyl-ester (L-NAME; 40 mg/kg per day for 14 days) plus Ang II (0 x 225 mg/kg per day on days 11-14); group 4, E(2) plus L-NAME/Ang II. |
| 252 | 20097717 | In vascular tissue (but not ventricular myocardium), caveolin-1 (cav-1) is the main component of caveolae; cav-1 modulates enzymes and receptors, such as the endothelial nitric oxide synthase and the angiotensin II (AngII) type 1 receptor. |
| 253 | 20375985 | Further, in both renal cells, visfatin synthesis was significantly increased by high glucose in the media but not by angiotensin II. |
| 254 | 20075747 | We analyzed whether fetal polymorphisms of the angiotensinogen (AGT) and angiotensin-converting enzyme genes influence birth weight and/or fetal total glycated hemoglobin (fTGH), a surrogate parameter of fetal insulin resistance at birth. |
| 255 | 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. |
| 256 | 20799102 | Patients in group 1 were exposed to less intensive pharmacological and interventional treatments (aspirin [93.6% vs. 95.3%; p = 0.012], clopidogrel [70% vs. 73%; p = 0.046], unfractionated heparin [59% vs. 65%; p <0.001], ACE inhibitors or angiotensin II antagonists [46% vs. 53%; p <0.001]). |
| 257 | 20601126 | We hypothesized that Ang II inhibits the anti-mitogenic pathways while enhancing the mitogenic pathways stimulated by insulin via activation of Protein Tyrosine Phosphatase-1B (PTP-1B) in VSMC. |
| 258 | 20601126 | We found that Ang II significantly inhibited insulin-induced phosphorylation of tyrosine 608 of IRS-1 and serine 473 of Akt, a downstream member of anti-mitogenic pathway of insulin. |
| 259 | 20601126 | In contrast, Ang II increased the serine phosphorylation of IRS-1 which was not affected by the presence of insulin. |
| 260 | 20601126 | Activation of p42/p44 MAPK (a mitogenic pathway) induced by insulin was further enhanced by Ang II. |
| 261 | 20601126 | Transfection of VSMC with PTP-1B antisense oligonucleotide markedly reduced the effects of Ang II on insulin signaling. |
| 262 | 20601126 | We conclude that Ang II modulates both anti-mitogenic and mitogenic pathways of insulin via the activation of PTP-1B. |
| 263 | 20667471 | Acute hyperglycemia increased synthesis of intrarenal Ang I and Ang II and resulted in activation of both Ang II receptors, AT1 and AT2, in the kidney. |
| 264 | 20667471 | Our data show that acute hyperglycemia stimulates Ang II synthesis in murine kidney cortex, this leads to AT2 activation and stimulation of VEGF mRNA translation, via the Akt-mTOR-p70(S6K) signaling pathway. |
| 265 | 20812878 | Aliskiren, the first approved renin inhibitor to reach the market, is a low-molecular-weight, orally active, hydrophilic non-peptide molecule that blocks angiotensin I generation. |
| 266 | 20851291 | There are reported associations between an angiotensin II type I receptor gene polymorphism (AT(1)R/A1166C) with hypertension, myocardial infarction, insulin resistance and cardiovascular disease risk. |
| 267 | 20666722 | Angiotensin II induces gene expressions of transforming growth factor (TGF)-? and matrix metalloproteinase (MMP)-9, and chymase also converts precursors of TGF-? and MMP-9 to their active forms. |
| 268 | 20666722 | In this model, the AAA development on an increase in MMP-9 activities induced by angiotensin II, but the inhibition of MMP-9 activation by chymase inhibitor resulted in attenuation of the AAA development. |
| 269 | 20666722 | Therefore, chymase inhibition may be useful for attenuating MMP-9 and TGF-? levels, in addition to reducing angiotensin II formation, and this function may provide powerful preventions of organ damages. |
| 270 | 20686488 | Furthermore, the H?O?-induced upregulation of angiotensinogen was inhibited by a mitogen-activated protein kinase (MAPK) kinase (MEK) inhibitor and a c-Jun N-terminal kinase (JNK) inhibitor, but not inhibited by a p38 MAPK inhibitor. |
| 271 | 20686488 | These data suggest that the majority of angiotensinogen was induced in mesangial cells in glomeruli under pathological conditions such as diabetic nephropathy, and angiotensinogen expression in mesangial cells was mediated by H?O? and the subsequent activation of extracellular-regulated kinase (ERK)/JNK pathways. |
| 272 | 20719975 | Here we assessed the effects of maximal RAS inhibition by angiotensin-converting enzyme (ACE) inhibitor plus angiotensin II type 1 receptor blocker (ARB) in combination with statin in rats with overt diabetic nephropathy. |
| 273 | 20739391 | Treatment of HK-2 cells with HG and ANG II also increased the protein-protein association between p-p66Shc and Pin1, an isomerase, in the cytosol, and with cytochrome c in the mitochondria. |
| 274 | 19114643 | Furthermore, MR antagonism substantially reduced the elevated NADPH oxidase activity and lipid peroxidation, expression of angiotensin II, angiotensin type 1 receptor, and MR in Ren2 vasculature. |
| 275 | 20819950 | Angiotensin II (Ang II) enhances ROS production by activating NAD(P)H oxidase and uncoupling endothelial nitric oxide synthase (NOS). |
| 276 | 20489655 | The experimental results showed that the cytotoxic effects of Ang II on human umbilical vein endothelial cells were significantly ameliorated by atorvastatin pretreatment (LDH tests, MTT assay, and propdium iodide (PI)/Annexin V-stating analysis), and atorvastatin treatment simultaneously enhanced expression of endothelial nitric oxide synthase and yielded of nitric oxide (NO) and cyclic guanosine monophosphate, but both effects were attenuated by the B2Rs antagonist HOE-140. |
| 277 | 20615910 | Baseline urinary angiotensinogen levels were positively correlated with renal angiotensinogen gene expression and AngII immunoreactivity but not with plasma renin activity or the urinary protein excretion rate. |
| 278 | 12092217 | Therapeutic possibilities in renin-angiotensin system control are offered by angiotensin-converting enzyme inhibitors, angiotensin II type-1 receptors antagonists, angiotensin converting enzyme inhibitors and neutral endopeptidase inhibitors and angiotensin II type 2 receptors agonists. |
| 279 | 18443229 | This effect of neuropeptide Y(1-36) was blocked by BIBP3226 (selective Y(1) receptor antagonist); Exogenous neuropeptide Y(3-36) did not enhance renovascular responses to angiotensin II. |
| 280 | 19765632 | The initial phase of ERK activation is due to HG itself and leads to AGT upregulation and the sustained phase is mediated for the most part by Ang II-activated AT1 receptor and leads to increased VEGF synthesis. |
| 281 | 19765632 | These data show that: (1) HG increases AGT synthesis and activation of renin and ACE by MCTs, leading to local production of Ang I and Ang II. (2) Ang II activates endogenous AT1 and stimulates synthesis of VEGF. (3) HG activation of ERK starts within minutes and lasts for up to 24h. |
| 282 | 19765632 | Early ERK activation is involved in AGT upregulation and sustained ERK activation, mediated via AT1, is responsible for VEGF synthesis. |
| 283 | 19350199 | In this study, we investigated the effects of APS treatment on cardiac function, myocardial collagen expression, cardiac ultrastructure, cardiac matrix metalloproteinase (MMP) activity, levels of plasma glycosylated serum protein (GSP), and myocardial enzymes, and the expression of Ang II, chymase, and angiotensin-converting enzyme (ACE) in the diabetic hamster myocardium. |
| 284 | 19350199 | Compared with insulin treatment, APS treatment significantly reduced myocardial collagen (type I and III) expression and lowered cardiac MMP-2 activity, myocardial Ang II levels, myocardial chymase expression, and p-ERK1/2 kinase expression. |
| 285 | 19350199 | In diabetic hamsters, myocardial ACE expression and plasma Ang II levels was not altered by insulin or APS treatment. |
| 286 | 21143167 | The favorable metabolic effects of telmisartan have been related to its Ang II receptor blockade and action as a partial agonist of peroxisome proliferators activated receptor (PPAR)-?. |
| 287 | 21177830 | Compared with Zucker lean, ZO controls exhibited increased proteinuria and ?-glutamyl transpeptidase, reductions in systemic insulin sensitivity in association with increased renal renin, (pro)renin receptor, angiotensin II type 1 receptor, and mineralocorticoid receptor immunostaining, oxidative stress, and glomerular tubular structural abnormalities that were substantially improved with in vivo nebivolol treatment. |
| 288 | 20676904 | ANG II and PE significantly increased levels of ANP and ?-actin and phosphorylation of p38 and ERK in the non-diabetic but not in the diabetic group; phosphorylation of Akt was unchanged irrespective of group or treatment. |
| 289 | 20945395 | Moreover, HG induced gene expression of angiotensinogen, renin, AT(1) R, and angiotensin II (Ang II) synthesis were inhibited by RAR? agonists and promoted by silencing RAR?. |
| 290 | 20945395 | Activation of RXR?, downregulated the expression of AT(1) R; and RXR? silencing accelerated HG induced expression of angiotensinogen and Ang II synthesis, whereas there was no significant effect on renin gene expression. |
| 291 | 21153603 | This study investigated whether elevated Angiotensin II influences myocardial insulin resistance, insulin signaling and NO production in a rat model of diet-induced obesity (DIO) by antagonizing the actions of the AT1 receptor with Losartan. |
| 292 | 21153603 | We conclude that Angiotensin II signaling exacerbates inhibition of NO production in insulin resistance and that this can be improved by AT1 antagonism. |
| 293 | 20418269 | At variance with angiotensin-converting enzyme (ACE) inhibitors, aliskiren eliminates the main substrate for the 'escape' phenomenon (synthesis of angiotensin II from angiotensin I through alternative enzymatic pathways). |
| 294 | 21263116 | Interestingly, the sympathetic response to insulin was eliminated by PVN injection of the melanocortin 3/4 receptor antagonist SHU9119, but was unaffected by the angiotensin II type 1 receptor antagonist losartan. |
| 295 | 10751221 | It has been shown that glomerular ANG II receptors are downregulated and protein kinase C (PKC) activity is enhanced in diabetes mellitus. |
| 296 | 11208601 | The interaction of ANG II with intrarenal AT1 receptors has been implicated in the progression of diabetic nephropathy, but the role of intrarenal AT2 receptors is unknown. |
| 297 | 11208601 | Our data suggest that alterations in the balance of kidney AT1 and AT2 receptor expression may contribute to ANG II-mediated glomerular injury in progressive diabetic nephropathy. |
| 298 | 12372774 | The lipoxygenase (LO) pathway of arachidonate metabolism and mitogen-activated protein kinases (MAPKs) can mediate cellular growth and ANG II effects in vascular smooth muscle cells. |
| 299 | 12372774 | ANG II and 12(S)-HETE led to activation of p38(MAPK) and its target transcription factor cAMP-responsive element-binding protein (CREB). |
| 300 | 12372774 | ANG II- and 12(S)-HETE-induced CREB activation and [(3)H]leucine incorporation were blocked by the p38(MAPK) inhibitor SB-202190. |
| 301 | 12372774 | Thus p38(MAPK)-dependent CREB activation may mediate ANG II- and LO product-induced FN expression and cellular growth in rat MC. |
| 302 | 14678947 | Clinical and animal studies show that treatment with angiotensin-converting enzyme (ACE) inhibitors or ANG II-receptor antagonists slows progression of nephropathy in diabetes, indicating ANG II plays an important role in its development. |
| 303 | 14678947 | We hypothesized that the ACE inhibitor captopril and the ANG II-receptor antagonist candesartan would hinder hyperglycemic-induced activation of JAK and STAT proteins in rat glomeruli, demonstrating that ANG II plays an important role in the activation of these proteins in vivo. |
| 304 | 16954340 | All five acute interventions caused significant increases of PRC in both COX-2+/+ and -/- mice, but the response was consistently less in COX-2-deficient mice (e.g., DeltaPRC in ng ANG I x ml(-1) x h(-1) caused by furosemide, isoproterenol, hydralazine, quinaprilate, or candesartan 4,699 +/- 544, 3,534 +/- 957, 2,522 +/- 369, 9,453 +/- 1,705, 66,455 +/- 21,938 in 129J WT, and 201 +/- 78, 869 +/- 275, 140 +/- 71, 902 +/- 304, 2,660 +/- 954 in 129J COX-2-/-). |
| 305 | 18216149 | Exposure to high glucose resulted in a 2.1-fold increase ANG II levels mediated through increased renin activity, as exposure to high glucose increased renin levels and preincubation with Aliskiren abrogated glucose-induced ANG II production. |
| 306 | 18400871 | We hypothesized that COX2 inhibition would be associated with preferential vasoconstriction in women and would augment their response to ANG II. |
| 307 | 18400871 | Baseline renal function and the response to an ANG II infusion were assessed during clamped euglycemia, and again after COX2 inhibition (200 mg celecoxib daily for 14 days) in 12 men and 9 women after 1 wk on a controlled protein and sodium diet. |
| 308 | 18400871 | Before COX2 inhibition, women exhibited a decline in glomerular filtration rate in response to ANG II. |
| 309 | 18768589 | Visfatin synthesis was markedly increased, not by angiotensin II, but by high glucose stimuli. |
| 310 | 19846569 | Although renal cortical ACE protein activity [2.1 +/- 0.8 vs. 9.2 +/- 2.1 arbitrary fluorescence units (AFU) x mg(-1) x min(-1)] and intensity of immunohistochemical staining were significantly reduced and ACE2 protein activity (16.7 +/- 3.2 vs. 7.2 +/- 2.4 AFU x mg(-1) x min(-1)) and intensity elevated, kidney ANG I (113 +/- 24 vs. 110 +/- 45 fmol/g) and ANG II (1,017 +/- 165 vs. 788 +/- 99 fmol/g) levels were not different between diabetic and control mice. |
| 311 | 19846569 | In control kidneys, afferent arteriole vasoconstriction produced by ANG I was significantly attenuated by ACE inhibition, but not by serine protease inhibition. |
| 312 | 19846569 | In contrast, afferent arteriole vasoconstriction produced by intrarenal conversion of ANG I to ANG II was significantly attenuated by serine protease inhibition, but not by ACE inhibition in diabetic kidneys. |
| 313 | 20627940 | The aim of this study was to evaluate angiotensin-I converting enzyme (ACE) activity and expression in numerous tissues, especially kidney, of non-obese diabetic mouse. |
| 314 | 16643859 | Since circulating glucagon and tissue angiotensin II (Ang II) levels are inappropriately elevated in type 2 diabetes, we tested the hypothesis that glucagon induces phosphorylation of ERK 1/2 in MCs by interacting with Ang II receptor signaling. |
| 315 | 20948237 | Renin exhibits profibrotic actions independent of angiotensin II, which is regulated by extracellular signal-regulated kinase 1 and 2 (ERK1/2). |
| 316 | 20374254 | Because DPPIV inhibitors are often used in metabolic syndrome, it is important to determine whether DPPIV inhibition in this setting enhances renovascular responses to AngII. 2. |
| 317 | 21182486 | The fact that a number of chemically unrelated drugs, such as angiotensin II antagonists, selective beta- 1 adrenergic antagonists, plant phenolics, statins, and farnesoid X receptor agonists have all been found to reduce dimethylarginine levels in plasma or tissue allows for an integrated study. |
| 318 | 20814220 | In addition, high glucose stimulated angiotensinogen and renin expression, increased renin activity, and resulted in increased angiotensin II formation. |
| 319 | 21668039 | Among different drug classes, angiotensin II type 1 receptor antagonists (angiotensin receptor blockers [ARBs]) have provided an excellent alternative to ACE inhibitors, representing a more selective and a better tolerated pharmacological approach to interfere with the RAS. |
| 320 | 20383279 | Angiotensin II (Ang II) plays a major role in the pathogenesis of insulin resistance and diabetes by inhibiting insulin's metabolic and potentiating its trophic effects. |
| 321 | 20383279 | We found Ang II to block insulin-dependent GLUT4 translocation in L6 myotubes in an NO- and O(2)(*-)-dependent fashion suggesting the involvement of peroxynitrite. |
| 322 | 20383279 | This hypothesis was confirmed by the ability of Ang II to induce tyrosine nitration of the MAP kinases ERK1/2 and of protein kinase B/Akt (Akt). |
| 323 | 20383279 | Inhibition of nitric oxide synthase and NAD(P)Hoxidase and scavenging of free radicals with myricetin restored insulin-stimulated Akt phosphorylation and GLUT4 translocation in the presence of Ang II. |
| 324 | 20383279 | Taken together, our data show that Ang II inhibits insulin-mediated GLUT4 translocation in this skeletal muscle model through at least two pathways: first through the transient activation of ERK1/2 which inhibit IRS-1/2 and second through a direct inhibitory nitration of Akt. |
| 325 | 21721600 | Use of combination pharmacotherapy, including angiotensin-converting enzyme (ACE) inhibitors, angiotensin II type 1 receptor antagonists (angiotensin receptor blockers) and ?-adrenoceptor antagonists (?-blockers) in the management of heart failure (HF) can reduce mortality, prevent functional decline and reduce health service use. |
| 326 | 21729002 | Exercise, through laminar shear stress activation, down-regulates endothelial AT1R (angiotensin II type 1 receptor) expression, leading to decreases in NADPH oxidase activity and superoxide anion production, which in turn decreases ROS (reactive oxygen species) generation, and preserves endothelial NO bioavailability and its protective anti-atherogenic effects. |
| 327 | 21314328 | We used real-time polymerase chain reaction to detect mRNA expression of renin, angiotensinogen (AGT), angiotensin-converting enzyme (ACE), angiotensin II (Ang II) type 1 receptor (AT1), and Ang II type 2 receptor (AT2); western blot analysis for expression of ANG and AT1; and radioimmunoassay to measure Ang II production from MCs in the supernatants of culture media. |
| 328 | 21314328 | Visfatin treatments increased renin, angiotensinogen (AGT), AT1 mRNA, and AGT, AT1 protein expression, as well as Ang II levels in a dose-dependent manner but did not affect ACE and AT2 mRNA levels in cultured rat MCs. |
| 329 | 21306748 | The purpose of this study was to clarify the association of the angiotensinogen gene (AGT) with insulin sensitivity using single nucleotide polymorphism (SNP) and haplotype analyses in a white cohort. |
| 330 | 19348235 | On the other hand, RAA system activates the insulin resistance by angiotensin II (Ang II) blocking effects of the intracellular signal transduction system of insulin, by oxidative stress and by reduction of adiponectin level, which effects are induced by Ang II. |
| 331 | 21747283 | Ang II infusion induces skeletal muscle atrophy in rodents and mechanisms include increased expression of the E3 ligases atrogin-1/MuRF-1, an elevated rate of ubiquitin-proteasome mediated proteolysis and increased reactive oxygen species (ROS) levels, closely mimicking conditions of human cachexia. |
| 332 | 21747283 | Nicotinamide adenine dinucleotide phosphate oxidase- and mitochondria-derived ROS contribute to ang II-induced oxidative stress. |
| 333 | 21793336 | Furthermore, results of RT-PCR and immunohistochemistry showed that Piog administration reduced angiotensin II type 1 receptor (AT1-R) expression in diabetic models. |
| 334 | 21525005 | In addition, the Crh gene promoter was significantly transactivated via the cAMP-responsive element by angiotensin II stimulation. |
| 335 | 21454245 | Angiotensin II has been implicated in a number of pathophysiologic processes with the potential to indirectly or directly influence the pathogenesis of insulin resistance and type 2 diabetes. |
| 336 | 21487074 | Diabetes also significantly increased NADPH oxidase (NOX) expression and protein nitration along with upregulation of angiotensin II (Ang II) and its receptor expression. |
| 337 | 21487074 | These results suggest that Ang II plays a critical role in diabetic lung fibrosis, which is most likely caused by NOX activation-mediated nitrosative damage. |
| 338 | 21519965 | This was not attributable to differences in potassium or angiotensin II, as glucose-stimulated insulin secretion was enhanced in As (-/-) mice even during high sodium intake. |
| 339 | 21846157 | In this review, we provide a brief overview of the renin-angiotensin-aldosterone system (RAAS) and discuss the rationale, clinical evidence, and shortcomings related to the use of angiotensin-converting enzyme (ACE) inhibitors in combination with angiotensin II type 1 receptor antagonists (angiotensin receptor blockers [ARBs]). |
| 340 | 21846157 | DRIs may be useful in combination with ACE inhibitors or ARBs as they provide a more complete blockade of the RAAS, effectively suppressing residual angiotensin II production and the counter-regulatory increase in plasma renin activity observed in patients receiving monotherapy with ACE inhibitors or ARBs. |
| 341 | 21929289 | In our study, we examined the role of PKC and PDGF receptor on JAK2 and STAT1 phosphorylation under high glucose (HG) condition (25 mmol/L) in response to Ang II in cultured vascular smooth muscle cells (VSMC). |
| 342 | 21929289 | High glucose markedly increased the phosphorylation of tyrosine residues of JAK2 and serine residues of STAT 1 compared with cells cultured in NG (5.5 mmol/L) with and without Ang II stimulation. |
| 343 | 21949629 | Direct renin inhibitors (DRIs) inhibit plasma renin activity (PRA), thereby preventing the conversion of angiotensinogen to angiotensin I; consequently, the levels of both Ang I and Ang II are reduced. |
| 344 | 21977024 | In conditions of over-nutrition, increased insulin (INS) and angiotensin II (Ang II) activate mammalian target for rapamycin (mTOR)/p70 S6 kinase (S6K1) signaling, whereas chronic alcohol consumption inhibits mTOR/S6K1 activation in cardiac tissue. |
| 345 | 21124341 | RAS activity was assessed by plasma renin activity, and evaluation of the vascular sensitivity to angiotensin II (AngII) using the mean arterial pressure (MAP) response to an infusion of AngII. |
| 346 | 21945916 | Whereas angiotensinsinogen, angiotensin converting enzyme (ACE), Ang I and Ang II are synthesized within these tissues, there is still controversy as to whether renin is produced locally or whether it is taken up from the circulation, possibly by the (pro)renin receptor. |
| 347 | 21716327 | Interleukin-6 (IL-6) has been implicated in animal studies to play an important role in angiotensin II (ANGII)-mediated hypertension. |
| 348 | 21950781 | Recently, besides the well known therapeutic approaches for RAS blockade, based on the use of ACE inhibitors, angiotensin II type 1 receptor antagonists (angiotensin receptor blockers [ARBs]) and aldosterone antagonists, both the scientific and medical community have focused their attention on a novel therapeutic option. |
| 349 | 18678790 | This study was undertaken to elucidate the role of angiotensin II and apoptosis signal regulating kinase-1 (ASK1) in obesity/diabetes-associated cardiovascular complications and hepatic steatosis. |
| 350 | 20384568 | No previous study has investigated how the vaso-constrictive peptide Ang II impacts insulin action in isolated mammalian skeletal muscle. |
| 351 | 20384568 | Soleus strips were incubated with insulin (5 mU/ml) and/or Ang II (500 nM) for 2 hours. |
| 352 | 20384568 | Ang II caused significant (p < 0.05) inhibition of insulin-stimulated glucose transport (39%) and decreased phosphorylation of Akt Ser(473) (37%) and glycogen synthase kinase-3beta Ser(9) (42%) without affecting phosphorylation of IRS-1 Ser(307) or p38 MAPK. |
| 353 | 21941204 | Urinary renin, therefore, more closely reflects renal RAAS activity than urinary angiotensinogen or aldosterone. |
| 354 | 21880378 | At a cellular level, angiotensin II (Ang II) and aldosterone induce insulin resistance by increasing oxidative stress and altering insulin signaling, leading to decreased glucose transport. |