Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0406810 (NAME)
 13,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the present study was to analyse quantitatively, on a cat gastrocnemius preparation in vivo, the effects of i.a. or i.v. administered glyceryl trinitrate (GTN), sodium nitroprusside (SNP) or nitric oxide (NO dissolved in saline) on vascular resistance (tone) in the following consecutive vascular sections: Large-bore arterial resistance vessels (> 25 microns), small arterioles (< 25 microns), and the veins. Effects on hydrostatic capillary pressure (Pc,v) and transcapillary fluid exchange were simultaneously recorded. Close-arterially infused GTN (1-4096 micrograms kg tissue-1 min-1), SNP (0.5-32 micrograms kg tissue-1 min-1) and NO (0.14-0.82 mg kg tissue-1 min-1) elicited a generalized dose-dependent dilator response in all three sections, though with a preferential action on the arterial side. Further, these agents caused an increase in Pc,v and transcapillary fluid filtration. The sites of action along the vascular bed of these exogenous vasodilators differed from that previously established for endogenous EDNO. Infusion of GTN, SNP and NO during EDNO blockade (L-NAME) could, therefore, not restore the vascular resistance distribution to that prevailing in the initial control state. Myogenic vascular reactivity to standardized transmural pressure stimuli was clearly depressed by GTN and SNP. Intravenously infused GTN (4-512 micrograms kg body wt-1 min-1) and SNP (4-64 micrograms kg body wt-1 min-1) decreased arterial pressure and elicited, via reflex sympathetic activation, a dose-dependent vasoconstriction in skeletal muscle, a decrease in Pc,v, and net transcapillary fluid absorption. The constrictor response thus overruled the direct dilator effect of the drugs. The plasma volume expansion known to result from long-term systematic administration of nitrovasodilators seems in part to be caused by transcapillary fluid absorption in skeletal muscle.
Acta Physiol Scand 1994 Sep
PMID:Effects of glyceryl trinitrate, nitroprusside and nitric oxide on arterial, venous and capillary functions in cat skeletal muscle in vivo. 781 Mar 36

The quantitative relationship between, increase in blood flow and arterial diameter was determined in an anaesthetized dog preparation (pentobarbitone, induction 30 mg kg-1 i.v., maintenance 3 mg kg-1 i.v. every 30 min). Changes in external iliac artery diameter were measured using piezoelectric ultrasound transducers capable of measuring diameters within the range of 2-20 mm with a resolution of +/- 0.005 mm. The diameter of the artery was measured at two sites, at one of which the endothelium was damaged using a balloon angioplasty catheter. Increases in blood flow were brought about by a combination of vasodilatation and cardiac stimulation (intra-arterial administration of acetylcholine, downstream to the sites of diameter measurement, and electrical stimulation of the left ansa subclavia), thereby preventing large changes in blood pressure. The effects of both transient and maintained increases in blood flow on mean arterial diameter in the section of artery with intact endothelium were measured. Transient increases in mean flow from 147 +/- 0.21 to 611 +/- 80.0 ml min-1 caused increases in diameter of 0.12 +/- 0.02 mm from a control of 5.42 +/- 0.19 mm. The mean delay between maximum flow and maximum diameter was 24.51 +/- 1.1 s and the half-time for the return to control diameter was 82.0 +/- 9.6 s, compared with 12.1 +/- 1.5 s for the return to control flow. Maintained (3-4 min) increases in mean blood flow (from 104.7 +/- 15.1 to 694.7 +/- 135.1 ml min-1) produced larger increases in diameter of 0.48 +/- 0.30 mm from a control diameter of 4.89 +/- 0.12 mm. These changes in diameter were abolished by N omega-nitro-L-arginine methyl ester (L-NAME. 10-100 mg kg-1 i.v.). In the section of artery with damaged endothelium, changes in diameter were relatively small and associated with small changes in blood pressure. This effect of a nearly 7-fold increase in flow on arterial diameter is dependent upon the integrity of the endothelium and the release of endothelium-derived relaxing factor and causes a 29% reduction in calculated boundary wall shear stress.
Exp Physiol 1994 Sep
PMID:The relationship between blood flow and diameter in the iliac artery of the anaesthetized dog: the role of endothelium-derived relaxing factor and shear stress. 781 56

Instillation of carbachol (150 micrograms/kg) into the gastric lumen in vivo increased the thickness of the mucus gel layer. Intravenous administration of the inhibitor of nitric oxide (NO) synthase, NG-nitro-L- arginine methyl ester (L-NAME, 0.4-5 mg/kg) dose-dependently reduced the stimulation by carbachol, the half-maximal inhibitory dose being 0.57 mg/kg. This effect of L-NAME was abolished by administration of L-arginine but not by D-arginine (100 mg/kg i.v.). By contrast L-NAME (5 mg/kg) did not reduce the stimulatory effect of intraluminal 16,16-dimethyl prostaglandin E2 (50 micrograms/kg) on mucus gel thickness. These results implicate NO in the cholinergic activation of gastric mucus secretion.
Eur J Pharmacol 1994 Sep 22
PMID:Stimulation by carbachol of mucus gel thickness in rat stomach involves nitric oxide. 782 53

1. N omega-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO biosynthesis, which blocks basal NO production, caused a similar increase of mean arterial pressure (MAP) in control hyper- and hypothyroid rats at the lowest dose, however, smaller pressor effects were observed with increasing doses in hyper- and hypothyroid rats. An additional dose of L-NAME (30 mg/kg), which produced no further increase in pressure, killed 90% of the hyperthyroid rats, whereas hypothyroid and control rats survived this additional dose. 2. The systemic responses to acetylcholine (ACh), an endothelium-dependent vasodilator that stimulates NO production/release, were significantly increased in hypothyroid rats, while hyperthyroid rats showed no significant differences when compared with controls. However, 10(-8) M ACh killed hyperthyroid rats, whereas control and hypothyroid rats survived this dose. 3. The maximal hypotensive response to sodium nitroprusside (SNP), an agonist that generates NO, was similar in intact controls, hyper- and hypothyroid rats. 4. These data indicate that hyper- and hypothyroidism show a reduction in basal NO synthesis/release, this reduced systemic NO tone being essential for life in hyperthyroid rats; whereas the response to ACh is not reduced and the hypotensive response to SNP did not differ between groups, indicating that the responsiveness of the systemic circulation to NO is not altered in either thyroid disorder.
Gen Pharmacol 1994 Sep
PMID:Role of nitric oxide in the systemic circulation of conscious hyper- and hypothyroid rats. 783 32

1. The present study was undertaken to determine whether endothelial nitric oxide (NO) is involved in the endothelium-dependent vasodilation elicited by bradykinin (BK) in rings of newborn (1-7-day-old) piglet cerebral arteries precontracted with KCl (25 mM). 2. In these rings, BK (10(-10)-10(-6) M) induced concentration-dependent relaxation. The preincubation with the precursor of NO synthesis, L-arginine (10(-4) M), reduced KCl-induced contraction and increased the BK relaxation. However, preincubation with the NO synthase inhibitor, NG-nitro-L-arginine-methyl ester (L-NAME; 3 x 10(-5) M), increased KCl contraction and basal tone, and inhibited BK relaxation. 3. These results suggest that the endothelium of these arteries possesses the ability to produce NO, either basal or stimulated by agents like BK.
Gen Pharmacol 1994 Sep
PMID:Role of nitric oxide on the endothelium-dependent vasodilation in newborn piglet cerebral arteries. 783 34

We assessed the effects of the inhibition of endogenous nitric oxide (NO) synthesis with Nw-nitro-L-arginine methyl ester (L-NAME) on water and sodium handling after NaCl load containing the inhibitor at 0, 0.5, 5 and 50 mg/kg in conscious control, hyper- and hypothyroid rats. L-NAME at 0.5 mg/kg caused a similar decrease in diuresis and natriuresis in control and hypothyroid rats, whereas no changes were seen in the hyperthyroid group. The saline load with 5 mg/kg of L-NAME produced no significant changes with respect to the 0 dose in any variable in control and hypothyroid rats, but increased natriuresis in the hyperthyroid group. The highest dose of L-NAME (50 mg/kg) increased the diuretic and natriuretic response in control and hyperthyroid groups, whereas in the hypothyroid group no urinary variable was significantly modified with respect to the 0 dose. These results indicate that the antidiuretic and antinatriuretic effects of L-NAME at low doses are suppressed in hyperthyroid rats, whereas the diuretic and natriuretic effects at high doses are absent in hypothyroid rats. Our findings suggest that the modulatory role of NO on sodium and water excretion is affected in both thyroid disorders. In addition, the highest dose of L-NAME killed hyperthyroid rats, indicating that NO plays an essential role for life in hyperthyroidism.
Horm Metab Res 1994 Sep
PMID:Effects of Nw-nitro L-arginine methyl ester on the response to NaCl load in hyper- and hypothyroid rats. 783 23

In the present experiments we planned to ascertain whether an abnormal production of nitric oxide (NO) by human CHP100 neuroblastoma cells in culture following stimulation of N-methyl-D-aspartate (NMDA) receptors, produced lethal effects in co-cultured human BMEL melanoma cells. Human BMEL melanoma cells in culture were found to be positive to the nicotinamide adenine dinucleotide phosphate diaphorase (NADPH diaphorase) histochemical reaction and produced NO as revealed by measurements of nitrite under basal culture conditions. Exposure for 50 min to aspartate (1-2 mM) or to NMDA (0.5-1.5 mM) did not evoke significant melanoma cell death. The dose of 1.0 mM NMDA applied for 1 min to BMEL cell cultures did not increase significantly nitrite concentrations in comparison to controls. Incubation for 50 min of human CHP100 neuroblastoma cells with NMDA (0.5-1.5 mM) elicited dose-dependent death of BMEL melanoma cells co-cultured in trans-wells. Under these experimental conditions, nitrite levels in cell culture-inserts containing melanoma cells increased by 120% 1 min after application of the excitotoxin (1 mM) to CHP100 neuroblastoma cultures. The lethal effects produced in BMEL cell culture-inserts by application of NMDA (1.0 mM) to CHP100 cultures were prevented by pretreatment of neuroblastoma cultures with MK801 (200 nM). Similar protection was also afforded by N omega-nitro-L-arginine methyl ester (L-NAME; 0.2 mM) and N omega-monomethyl-L-arginine (L-NMMA; 0.2 mM), two inhibitors of nitric oxide synthase, and by haemoglobin (10 microM), a nitric oxide trapping agent.(ABSTRACT TRUNCATED AT 250 WORDS)
Neuropharmacology 1994 Sep
PMID:N-methyl-D-aspartate-induced excessive formation of nitric oxide in CHP100 neuroblastoma cells produces death of BMEL melanoma cells in co-culture. 783 19

Experiments were performed to investigate the role of nitric oxide (NO) in the regulation of joint blood flow and in modulating sympathetic vasoconstrictor influences in normal and acutely inflamed rabbit knees. Close intra-arterial infusion of N omega-nitro_L-arginine methyl ester (L-NAME), a NO production inhibitor, reduced basal joint blood flow, measured by laser Doppler flowmetry, by 36.4 +/- 5.1% (mean +/- S.E.M.) in normal (control) and 21.4 +/- 7.8% in carrageenan-inflamed knee joints. Mean systemic arterial blood pressure was increased by 20 +/- 3.1 and 17.9 +/- 2% in control and test animal groups respectively. Joint vascular resistance was increased by 101 +/- 19% in normal and 68.9 +/- 13.7% in carrageenan-treated animals. Vasoconstrictor responses to electrical stimulation of the posterior articular nerve (PAN) were significantly smaller in the inflamed joint compared to normal. Infusion of L-NAME for 45 min resulted in an increased vasoconstrictor response by 78% in normal and 79% in inflamed joints. Subsequent close intra-arterial infusion of L-arginine failed to return the enhanced vasoconstrictor responses induced by L-NAME to their control levels in both normal and test animal groups, but partially restored blood flow changes. In both normal and inflamed joints, vasoconstriction produced by separate intra-arterial injection of the alpha 1-agonist phenylephrine (2.5 nmol) or either of the alpha 2-agonists clonidine (250 pmol) and UK-14304 (250 pmol) was increased significantly by L-NAME infusion but not completely restored to basal values by L-arginine infusion. The control responses to all three agents did not differ significantly between normal and inflamed knees.(ABSTRACT TRUNCATED AT 250 WORDS)
Exp Physiol 1993 Sep
PMID:Nitric oxide modulates sympathetic vasoconstriction and basal blood flow in normal and acutely inflamed rabbit knee joints. 790 8

The present study was designed to investigate the role of the autonomic nervous system in experimental hypertension induced by chronic administration of N-nitro-L-arginine methyl ester (L-NAME) in the drinking water (1 mg/mL) over 6 days. L-NAME ingestion caused a large rise in resting mean arterial pressure (MAP) (175 +/- 5 mm Hg) and heart rate (HR) (440 +/- 17 beats per minute) compared to nontreated control rats (resting MAP: 112 +/- 2 mm Hg and HR: 345 +/- 8 beats per minute). Ganglionic blockade induced by trimethaphan (5 mg/kg, intravenously) caused a significantly (P < .01) greater decrease in MAP (delta -86 +/- 7 mm Hg) compared to control rats MAP (delta -44 +/- 4 mm Hg). This strongly suggests that the level of central sympathetic tone in L-NAME-treated rats is much greater than in nontreated rats. Using atenolol and atropine alone and combined, the level of resting sympathetic drive to the heart was found to be significantly increased in L-NAME-treated rats compared to control rats. However, vagal tone to the heart was found to be virtually abolished in L-NAME-treated rats compared to control rats. These results indicate that an increase in central sympathetic drive plays an important role in the hypertension induced by chronic inhibition of nitric oxide synthesis with L-NAME.
Am J Hypertens 1993 Sep
PMID:Evidence that the autonomic nervous system plays a major role in the L-NAME-induced hypertension in conscious rats. 790 20

Studies were undertaken in the rat isolated renal artery in order to determine if adenosine receptor agonists were capable of inducing the release of nitric oxide from the renovascular endothelium. N6-cyclopentyladenosine (CPA) and 5'-N-ethylcarboxamidoadenosine (NECA) produced concentration-dependent relaxations in endothelium intact renal artery rings. The NECA curve was biphasic with a first phase pA50 of 6.05. The CPA curve was monophasic with a pA50 of 4.35. In the absence of endothelium the curves to both NECA and CPA were monophasic with pA50 values of 3.37 and 3.50, respectively. The A2a adenosine receptor-selective agonist CGS21680 (2-[p-(2-carboxyethyl)-phenethylamino]-5'-N-ethylcarboxamidoadenos ine) was inactive in endothelium intact tissues. Relaxant responses to CPA and NECA in the presence of endothelium were antagonized by 8-p-sulfophenyltheophylline and by 1,3-dipropyl-8-cyclopentylxanthine only at a nonselective concentration (3 x 10(-6) M) suggesting activation of A2 adenosine receptors. The responses to CPA and NECA in the absence of endothelium are not due to activation of A1 or A2 adenosine receptor subtypes because they are resistant to blockade by these xanthines. CPA and NECA responses in the presence of endothelium were inhibited by NG-nitro-L-arginine methylester (L-NAME), a nitric oxide synthase inhibitor, but not by the cyclooxygenase inhibitor indomethacin or the K+ATP channel antagonist glibenclamide. These results suggest that the rat renal artery contains A2b adenosine receptors that are located exclusively on the endothelium and cause the release of nitric oxide.
J Pharmacol Exp Ther 1994 Sep
PMID:The endothelium of the rat renal artery plays an obligatory role in A2 adenosine receptor-mediated relaxation induced by 5'-N-ethylcarboxamidoadenosine and N6-cyclopentyladenosine. 793 1


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