Isolated perfused mesenteric arteries of portal vein ligated and sham-operated rats were contracted by methoxamine (3 nmol-3 mumol) and then treated with nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (100 microM), terlipressin or the selective V2 receptor agonist desmopressin (each 0.5 uM). Terlipressin alone reduced and in combination with NG-nitro-L-arginine methyl ester abolished the difference in reactivity to methoxamine between the portal vein ligated and sham-operated groups ...

A role for the NO-cGMP pathway in mediating chemosensory activation of feeding is suggested by intense NADPH diaphorase staining observed in nerve fibers that project from sensory cells in the lips to the CNS and by the presence in the CNS of a NO-activated guanylyl cyclase. In preparations reduced to isolated lips and CNS, intracellular recordings were made from motoneurons driven by the interneurons of the central pattern generator (CPG) for feeding. Fictive feeding in such preparations can be recorded from these motoneurons following the application of sucrose to the lips. Sucrose activation of fictive feeding is inhibited by the NO scavenger hemoglobin, the NO synthase inhibitor N omega-Nitro-L-Arginine Methyl Ester (L-NAME) and by methylene blue, an inhibitor of guanylyl cyclase. Fictive feeding in isolated lip-CNS preparations can be activated without sucrose by superfusion of NO donor molecules such as SNAP and hydroxylamine and by the nonhydrolyzable analog of cGMP, 8-bromo-cGMP. The ...

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In the present study, chronic administration of bosentan, an antagonist of both ETA and ETB receptors, had no significant effect on the systolic BP level reached after 6 weeks of L-NAME treatment, confirming the observation that acute (60 minutes) administration of the selective ETA receptor antagonist BQ-123 could not lower BP in rats treated for 3 weeks with an l-arginine analogue.21 However, the delay in the BP elevation occurring when bosentan was added to L-NAME would suggest that ET is involved in the early hypertensive response to the l-arginine analogue. This observation is in line with studies showing a blunted hypertensive effect of acute L-NAME administrations by ET receptor antagonists12 13 14 and provides experimental evidence to explain the discrepancy in the efficacy of ET receptor antagonists in acute and chronic L-NAME-induced hypertension.. Chronic administration of L-NAME leads to eutrophic remodeling of the basilar artery, as we previously reported.15 The structural ...

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The purpose of this study was to examine the effects of nitric oxide on systemic hemodynamics and oxygen metabolism following acute hepatic inflow occlusion. Fourteen mongrel pigs received solvent (control group, n = 4), the nitric synthesis inhibitor NG-nitro-L-arginine methyl ester (L-NAME group, n = 5), or the substrate for nitric oxide synthesis L-arginine (L-arginine group, n = 5) 30 min before hepatic inflow occlusion. Following 30 min of hepatic ischemia, all livers were reperfused. While all pigs in the control group and L-arginine group survived more than 7 days after reperfusion, two of five pigs in the L-NAME group died during hepatic ischemia period. However, venous oxygen saturation was significantly lower during and after ischemic period, oxygen extraction ratio was significantly higher during hepatic ischemic period in L-NAME group, and systemic vascular resistance was also significantly higher 5 and 15 min after hepatic inflow occlusion. Furthermore, lactate/pyruvate ratio was ...

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Examination of the protective effect of L-NAME(N-Nitro L-Arginine Methyl Ester) and vitamin E (α-tocopherol) against oxidative stress caused by exposure of cigarette smoke to lungs in male rats ...

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TY - JOUR. T1 - Vaccination against the angiotensin type 1 receptor for the prevention of L-NAME-induced nephropathy. AU - Azegami, Tatsuhiko. AU - Sasamura, Hiroyuki. AU - Hayashi, Kaori. AU - Itoh, Hiroshi. PY - 2012/5. Y1 - 2012/5. N2 - Previous studies have shown that renin-angiotensin (Ang) system vaccines may be effective for the treatment of hypertension, but their efficacy for the prevention of renal disease is unclear. The aim of this study was to compare the effects of an Ang II type 1 (AT1) receptor vaccine with an Ang II receptor blocker (ARB) and a vasodilator on blood pressure (BP) and renal injury in the L-NAME nephropathy model. Male spontaneously hypertensive rats (SHRs) were divided into six groups and treated transiently with three injections of vehicle or AT1 receptor vaccine (0.1 mg) at age 4, 6 and 8 weeks, or continuously with candesartan cilexetil (0.1 mg kg -1 per day) or hydralazine hydrochloride (5 mg kg -1 per day), then administered NG-nitro-L-arginine methyl ester ...

Product Number , 58089751. CAS Number , 5874-57-7. EC , Molecular Formula , -. Molecular Weight , 155.58. Storage Temp , Harmonized Tariff code , Signal Word , ...

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The intracellular signaling of human urotensin II (hU-II) and its interaction with other vasoconstrictors such as ANG II are poorly understood. In endothelium-denuded rat aorta, coadministration of hU-II (1 nM) and ANG II (2 nM) exerted a significant contractile effect that was associated with increased protein kinase C (PKC) activity and phosphorylation of PKC-α/βII and myosin light chain, whereas either hU-II or ANG II administered alone at these concentrations had no statistically significant effect. This synergistic effect was abrogated by the PKC inhibitor chelerythrine (10 and 30 μM), the selective PKC-α/βII inhibitor Gö-6976 (0.1 and 1 μM), the hU-II receptor ligand urantide (30 nM and 1 μM), or the ANG II antagonist losartan (1 μM). Moreover, in endothelium-intact rat aorta, the synergistic effect of hU-II and ANG II was not exerted any longer, and this synergistic effect was unmasked by pretreatment of the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester. hU-II ...

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TY - JOUR. T1 - Linalool elicits vasorelaxation of mouse aortae through activation of guanylyl cyclase and K+ channels. AU - Kang, Purum. AU - Seol, Geun Hee. N1 - Publisher Copyright: © 2015 Royal Pharmaceutical Society.. PY - 2015/5/1. Y1 - 2015/5/1. N2 - Objectives The aim of this study was to investigate the cardiovascular relaxing properties of monoterpene alcohol (-)-linalool (LIN), a principal component of several aromatic plants. Methods We assessed the effects of LIN on vascular contractility in mouse aortae and evaluated its underlying mechanisms of action. Key findings We found that LIN dose-dependently relaxed the vascular tonus of mouse thoracic aortae induced by prostaglandin F2 alpha (PGF2α, 3 μm). This effect, however, was reduced by pretreatment with the nitric oxide synthase inhibitor L-NAME (30 μm). Treatment with the inhibitor of soluble guanylyl cyclase ODQ (2 μm) or the K+ channel blocker TEA (10 mM) partially blocked LIN-induced vasorelaxation. Moreover, addition of ...

Of all cancer types, prostate cancer is the second most common one with an age-standardized incidence rate of 29.3 per 100,000 men worldwide. Nitric oxide (NO) is both a radical and versatile messenger molecule involved in many physiological activities. NO was documented to be highly secreted and utilized by cancer cells. N omega-nitro-l-arginine methyl ester (L-NAME) is utilized for inhibiting NO synthase. Its worst long-term side effect is reported to be hypertension, hence less cytotoxic than chemotherapeutic agents. Herein, we carried out a cytotoxicity study on how different doses of L-NAME affect DU145 human prostate cancer cells. First, toxic doses of L-NAME were determined. Then, while antioxidant capacity was determined by glutathione and total antioxidant status, oxidative stress was evaluated by quantifying malondialdehyde, NO, and total oxidant status levels. Inflammatory effects of L-NAME were investigated by measuring tumor necrosis factor-alpha and interleukin-6 (IL-6) levels. ...

TY - JOUR. T1 - Effect of estrogen on cerebrovascular prostaglandins is amplified in mice with dysfunctional NOS. AU - Li, Xiangduan. AU - Geary, Greg G.. AU - Gonzales, Rayna J.. AU - Krause, Diana N.. AU - Duckles, Sue P.. PY - 2004/8. Y1 - 2004/8. N2 - Chronic estrogen treatment increases endothelial vasodilator function in cerebral arteries. Endothelial nitric oxide (NO) synthase (eNOS) is a primary target of the hormone, but other endothelial factors may be modulated as well. In light of possible interactions between NO and prostaglandins, we tested the hypothesis that estrogen treatment increases prostanoid-mediated dilation using NOS-deficient female mouse models, i.e., mice treated with a NOS inhibitor [NG-nitro-L-arginine methyl ester (L-NAME)] for 21 days or transgenic mice with the eNOS gene disrupted (eNOS-/-). All mice were ovariectomized; some in each group were treated chronically with estrogen. Cerebral blood vessels then were isolated for biochemical and functional analyses. In ...

This study was designed to assess the role of renin and of the sympathoadrenal system in the maintenance of the hypertension induced by chronic nitric oxide synthase (NOS) inhibition in rats kept on a normal (RS) or a low-sodium (LS) diet. With the administration of NG-nitro-L-arginine methyl ester (L-NAME) in drinking water (0.4 milligrams) for 6 wk, mean intra-arterial blood pressure rose to a similar extent to 201 mmHg in the RS and 184 mmHg in the LS animals. Simultaneously, plasma norepinephrine was increased to 838 and 527 pg/ml and epinephrine to 2,041 and 1,341 pg/ml in RS and LS, respectively. Plasma neuropeptide Y levels did not change. Plasma renin activity rose to 21 ng.ml-1.h-1 in RS but remained at 44 ng.ml-1.h-1 in the LS. Both losartan (10 mg/kg) and phentolamine (0.1 mg/kg) intravenous bolus injections reduced blood pressure considerably in the L-NAME hypertensive animals. Whole brain NOS activity was reduced by 84%. Hypertension induced by chronic NOS inhibition in LS

MACIEL, IZAQUE DE SOUSA... Nitric Oxide Synthase inhibition counteracts the stress-induced DNA methyltransferase 3b expression in the hippocampus of rats. European Journal of Neuroscience n. p. DEC 2020. Journal article.

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Previous studies identified a region on chromosome 1 associated with NG-nitro-L-arginine methyl ester (L-NAME) hypertension-induced renal disease in fawn-hooded hypertensive (FHH) rats. This region contains a mutant γ-adducin (Add3) gene that impairs renal blood flow (RBF) autoregulation, but its contribution to renal injury is unknown. The present study evaluated the hypothesis that knockout (KO) of Add3 impairs the renal vasoconstrictor response to the blockade of nitric oxide synthase and enhances hypertension-induced renal injury after chronic administration of L-NAME plus a high-salt diet. The acute hemodynamic effect of L-NAME and its chronic effects on hypertension and renal injury were compared in FHH 1Brown Norway (FHH 1BN) congenic rats (WT) expressing wild-type Add3 gene versus FHH 1BN Add3 KO rats. RBF was well autoregulated in WT rats but impaired in Add3 KO rats. Acute administration of L-NAME (10 mg/kg) raised mean arterial pressure (MAP) similarly in both strains, but RBF and ...

ABSTRACT Objective: To evaluate the role of nitric oxide (NO) in pioglitazone (PIO) mediated anti-inflammatory activity in ulcerative colitis. Material and methods: Ulcerative colitis was induced in rats by intracolonical administration of 2, 4, 6-tri-nitrobenzene sulphonic acid (50mg/rat) after 10 days of initiation of treatment except in vehicle control group. Animals were randomly divided into five groups with six animals each. The groups received vehicle, TNBS, PIO, PIO+L-NAME (N-nitro-L-arginine methyl ester), L-NAME for 18 days respectively. PIO (25 mg/kg/day p.o) treatment for 18 days reduced mucosal damage induced by TNBS which was reflected by improvement in body weight, morphological grades of colon, reduced myeloperoxidase activity and histopathological studies. Administration of L-NAME (40 mg/kg/day, p.o) for 18 days in PIO+TNBS treated animals showed exaggerated mucosal damage as compared to PIO+TNBS treated animals. Results: Findings indicate that L-NAME altered the protective ...

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The present results showed that i.p. administration of IL-1β in freely moving rats induced a biphasic increase in mean arterial blood pressure, and that a rise in the plasma concentration of NOx occurred during the second phase of the pressor response (at 3 h after the injection of IL-1β). Furthermore, systemic pretreatment with DEX enhanced the second phase of the pressor response, thus confirming our previous finding (Watanabe et al., 1996), and inhibited the evoked increase in the plasma level of NOx. These results suggest that NO is involved as a vasodilator in the regulation of the late phase of the pressor response, and that the enhancement by DEX of the IL-1-induced rise in blood pressure was, at least in part, due to its inhibition of NO release. This idea is further supported by the finding that one of the most frequently used nonselective NOS inhibitors,l-NAME, both enhanced the IL-1β-induced pressor response and attenuated the NOx response seen in this study. This result indicates ...

ROSSI, Marcos Antonio. Chronic inhibition of no synthesis per se promotes structural animal remodeling of the rat aorta. Anais.. Washington: [s.n.], 2001 ...

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