Disease relevance of Ngamma-Nitro-L-arginine

• This activity could be inhibited by N-nitro-L-arginine methyl ester (L-NAME), a NO synthase inhibitor, and was stimulated by 15 min of hypoxia [1].
• Because in rats, inhibition of NO synthase with the L-arginine analogue N omega-nitro-L-arginine methyl ester (L-NAME) induces blood pressure elevation associated with little cardiovascular hypertrophy, we studied vascular endothelin-1 gene expression in L-NAME-treated rats and the effects of chronic endothelin antagonism [2].
• N-Nitro-L-arginine significantly inhibited the relaxation to hypercapnic acidosis but had no significant effect on relaxation to normocapnic acidosis [3].
• N omega-nitro-L-arginine administration corrects peripheral vasodilation and systemic capillary hypotension and ameliorates plasma volume expansion and sodium retention in portal hypertensive rats [4].
• In protocol 1, the administration of increasing doses (25, 50, 250, 500 and 1,000 micrograms.kg-1.min-1) of the nitric oxide biosynthesis inhibitor N omega-nitro-L-arginine to 18 conscious rats with cirrhosis and ascites produced, at each dose tested, a significantly greater increase in arterial pressure than in 17 conscious control rats [5].

Psychiatry related information on Ngamma-Nitro-L-arginine

• Moreover, no treatment effects were observed in the probe trials (i.e. after acquisition and after reversal learning), indicating that the rats treated with N omega-nitro-L-arginine had learned the spatial location of the platform [6].
• Once the motor activity was stabilized, N-nitro-L-arginine methyl-ester (L-NAME) was added to the bath at increasing concentration from 10(-7) to 10(-4) M [7].
• Here we show that injection of the nitric oxide synthase inhibitor N-nitro-L-arginine prior to training results in amnesia for the passive avoidance task; the amnesia can be overcome by injecting L-arginine along with the inhibitor [8].
• In contrast, N-omega-nitro-L-arginine (40 nmol, i.c.v.), an inhibitor of NO synthase, impaired spatial learning, but not passive avoidance learning [9].
• RESULTS: Intraperitoneal injection of 5 mg.kg(-1) N-nitro-L-arginine suppresses most of the withdrawal symptoms of morphine dependent rats [10].

High impact information on Ngamma-Nitro-L-arginine

• In vitro experiments indicated that NO synthase (NOS) inhibition by N-nitro-L-arginine methyl ester (L-NAME) enhanced IFN-gamma and TNF production by splenocytes in response to SEB [11].
• To determine the role of eNOS in mediating these effects, mice were treated with N-nitro-L-arginine methyl ester (L-NAME) [12].
• Immediately after birth, at 140 d of gestation, during the 3-h study period, mean pulmonary arterial pressure did not decrease in N omega-nitro-L-arginine-treated lambs; the increase in pulmonary blood flow and decrease in pulmonary vascular resistance were markedly attenuated compared to saline-treated lambs [13].
• Moreover, when the endogenous constitutive levels of NO made by endothelial cells are suppressed using N-omega-nitro-L-arginine, a potent competitive inhibitor of NO synthase, the baseline levels of ET-1 produced in normoxic environments are increased three- to fourfold [14].
• Nitric oxide synthesis by IL-1-activated smooth muscle cells is inhibited by NAA, NMA, and N omega-nitro-L-arginine (NNA) with ED50 (i.e., effective dose for 50% inhibition) values of 20, 60, and 1000 microM, respectively; this rank order of inhibition is characteristic of an agonist-unregulated, inducible isoform of nitric oxide synthase [15].

Chemical compound and disease context of Ngamma-Nitro-L-arginine

• Furthermore, HIV-1 Tat treatment significantly increased HBMEC permeability, and pretreatment with both N-nitro-L-arginine methyl ester and wortmannin inhibited the Tat-induced permeability [16].
• Similar experiments performed with the nonspecific NOS inhibitor N omega-nitro-L-arginine (NNA) also demonstrated an increased pressor sensitivity of the cirrhotic rats, but the arterial hypotension was completely corrected [17].
• Estrogen-induced vasodilation was not influenced either by pretreatment with N omega-nitro-L-arginine methyl ester (L-NAME) (100 mumol/liter intracoronary), indomethacin (5 mg/kg body weight intravenously), propranolol (0.75 mg/kg intravenously) or the classic estrogen receptor antagonist ICI 182,780 (10 mumol/liter) [18].
• Nitric oxide scavenging by hemoglobin or nitric oxide synthase inhibition by N-nitro-L-arginine induces cortical spreading ischemia when K+ is increased in the subarachnoid space [19].
• The nitric-oxide synthase (NOS) inhibitors 7-nitroindazole (7-NI) and N-omega-nitro-L-arginine methyl ester also reduced NMDA toxicity [20].

Biological context of Ngamma-Nitro-L-arginine

• To explore the involvement of NO in normal peristalsis, the effects of inhibitors of NO synthase, including N omega-nitro-L-arginine (L-NNA) and N omega-nitro-L-arginine methyl ester (L-NAME), on esophageal peristaltic contractions induced by diverse stimuli that may involve different neuronal circuits were studied [21].
• To verify the possible involvement of endothelium-derived relaxing factor (EDRF) in the alteration of NE-induced vasoconstriction after exercise training, we compared the vascular responses to NE in endothelium-intact, N omega-nitro-L-arginine (L-NNA, 10(-4) mol/L)-pretreated, or denuded vessel segments (n = 4 for each experiment of each group) [22].
• PGE2 as well as EP2- and EP4-attributed choroidal stimulation elicited greater vasorelaxation in the saline-treated newborn and was associated with higher nitrite (oxidation product of NO, N omega-nitro-L-arginine inhibitable) production than in adult tissues [23].
• Addition of N omega-nitro-L-arginine (NNLA), an inhibitor of NO synthesis, to the perfusion medium eliminated differences in coronary flow and oxygen consumption between normal and endotoxin-treated hearts [24].
• In control rats, N omega-nitro-L-arginine caused a decrease in estimated renal plasma flow without affecting glomerular filtration rate or sodium excretion [5].

Anatomical context of Ngamma-Nitro-L-arginine

• Mucus and alkali secretion in the rat duodenum: effects of indomethacin, N omega-nitro-L-arginine, and luminal acid [25].
• Recently, a new vasorelaxing factor, endothelium-derived hyperpolarizing factor (EDHF), which hyperpolarizes and relaxes the porcine coronary artery in the presence of N omega-nitro-L-arginine (NNA) and indomethacin (IM), has been reported [26].
• N omega-Nitro-L-arginine methyl ester (L-NAME, 10(-7) to 10(-4) mol/L) evoked marked endothelium-dependent contractions in coronary arteries (young, 52 +/- 8% of the contraction to 100 mmol/L KCl; adult, 40 +/- 8%) but not aortas (young, 3 +/- 1%; adult, 2 +/- 1%) [27].
• Superfusion of an inhibitor of NO synthase, N omega-nitro-L-arginine (NA; 1 mM), for 45 min abolished the increase of LCBF induced by topical bicuculline methiodide (10 mM) [164 +/- 18 ml/100 g per min in the artificial cerebrospinal fluid (aCSF)-superfused side and 104 +/- 12 ml/100 g per ml in the NA-superfused side; P < 0.005] [28].
• Chicken osteoclasts were cultured for 36 hr on bovine bone slices in the presence or absence of the NO-generating agent sodium nitroprusside or the NOS inhibitors N-nitro-L-arginine methyl ester and aminoguanidine [29].

Associations of Ngamma-Nitro-L-arginine with other chemical compounds

• With cells in L-Arg-free medium, we observed .O2- formation that increased as the cytosolic L-Arg levels decreased, while NO generation declined. .O2- formation was virtually abolished by the specific NOS blocker, N-nitro-L-arginine methyl ester (L-NAME) [30].
• Chemical removal of the vascular endothelium by perfusion with sodium deoxycholate (1.75 to 1.80 mg/mL) for 30 seconds and subsequent treatment with N omega-nitro-L-arginine (100 mumol/L) to inhibit nitric oxide synthesis abolished the initial rapid vasodilator action of ACh at any given concentration [31].
• In contrast, N omega-nitro-L-arginine administration to cirrhotic animals did not produce any appreciable renal vasoconstrictor effect, and it increased glomerular filtration rate and sodium excretion.(ABSTRACT TRUNCATED AT 250 WORDS)[5]
• In the presence of N omega-nitro-L-arginine, the change in total peripheral resistance after methoxamine infusion was similar in both groups (p greater than 0.05) [32].
• This O-2 formation required Ca2+/calmodulin and was blocked by the specific NOS inhibitor N-nitro-L-arginine methyl ester (L-NAME) but not its non-inhibitory enantiomer D-NAME [33].

Gene context of Ngamma-Nitro-L-arginine

• We found that the NO synthase inhibitor N-nitro-l-arginine methyl ester could reverse the inhibitory effects of VEGF on lymphocyte adhesion and EC cytoskeleton rearrangement [34].
• METHODS: We assessed: (1) effect of preconditioning on F16BP content; (2) effect of NO on GAPDH activity before and during sustained ischaemia; and (3) protective effect of F16BP in control, ischaemic, and preconditioned animals with or without administration of N-nitro-L-arginine methyl ester (L-NAME), NO donor, or F16BP [35].
• On day 6, mice were randomized to receive (a) PBS (control), (b) DC101 [VEGF receptor 2 (VEGFR-2) antibody] by i.p. injection, (c) N-nitro-l-arginine (NNLA; NOS inhibitor) in the drinking water, or (d) both DC101 and NNLA [36].
• The iNOS inhibitor N omega-nitro-L-arginine methyl ester increased B. suis multiplication specifically in IFN-gamma-treated cells infected with ops-Brucella, demonstrating a microbicidal effect of the NO produced [37].
• Oral administration of N omega-nitro-L-arginine methyl (from day 4 postinfection) increased mortality rates in both IL-5-/- and WT mice, indicating a protective role for nitric oxide during the early stages of oral T. gondii infection [38].

Analytical, diagnostic and therapeutic context of Ngamma-Nitro-L-arginine

• RESULTS: Electrical stimulation on the LES evoked inhibitory junction potentials (IJPs), which were reduced by 60% by 100 micromol/L N-nitro-L-arginine and subsequently blocked by 0.5 micromol/L apamin, unmasking excitatory junction potentials, which were abolished by 1 micromol/L hyoscine [39].
• METHODS AND RESULTS: Coronary vasomotor response was studied in pigs before and after chronic oral administration of the NO synthesis antagonist N omega-nitro-L-arginine methyl ester (L-NAME) 30 mg.kg-1.d-1 for 2 weeks [40].
• Partial portal vein-ligated or sham-operated rats were pretreated with a continuous intravenous infusion of either N omega-nitro-L-arginine (50 micrograms.kg-1.min-1) or saline [32].
• For 2 days before partial portal vein ligation or sham operation and then continuously for 4 days after the operation, animals received either placebo (0.9% saline) or N omega-nitro-L-arginine (approximately 2 micrograms/kg/min) intravenously through a subcutaneously implanted Alzet osmotic pump (model 2ML1; Alza, Palo Alto, CA) [4].
• Radiocontrast-induced nephropathy was produced in anesthetized rats (N = 6/group) by intravenous injection of indomethacin (5.0 mg/kg), the nitric oxide synthesis inhibitor N-nitro-L-arginine methyl ester (10.0 mg/kg), vehicle or antagonist, and the radiocontrast agent lopamidol (2,9 g iodine/kg) [41].

References