ArticleBritish journal of pharmacology2003
Comparative regional haemodynamic effects of the nitric oxide synthase inhibitors, S-methyl-L-thiocitrulline and L-NAME, in conscious rats.
Article in British journal of pharmacology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 36 citations in OpenAlex.
- Nitric oxide synthase inhibition with N(G)-monomethyl-l-arginine: Determining the window of effect in the human vasculature.Nitric oxide : biology and chemistry · 2020Article
- Article
- Acute Nitric Oxide Synthase Inhibition Accelerates Transendothelial Insulin Efflux In Vivo.Diabetes · 2018Article
- Neuronal nitric oxide synthase regulation of skeletal muscle functional hyperemia: exercise training and moderate compensated heart failure.Nitric oxide : biology and chemistry · 2018Article
- Blood Pressure in Healthy Humans Is Regulated by Neuronal NO Synthase.Hypertension (Dallas, Tex. : 1979) · 2017Article
- Nitric oxide production contributes to Bacillus anthracis edema toxin-associated arterial hypotension and lethality: ex vivo and in vivo studies in the rat.American journal of physiology. Heart and circulatory physiology · 2016Article
- Exercise training augments neuronal nitric oxide synthase-mediated inhibition of sympathetic vasoconstriction in contracting skeletal muscle of rats.The Journal of physiology · 2014Article
- Administration of S-methyl-L-thiocitrulline protects against brain injuries after intracerebral hemorrhage.Neuroscience · 2014Article
- Muscle fibre-type dependence of neuronal nitric oxide synthase-mediated vascular control in the rat during high speed treadmill running.The Journal of physiology · 2013Article
- Neuronal nitric oxide synthase inhibition and regional sympathetic nerve discharge: implications for peripheral vascular control.Respiratory physiology & neurobiology · 2013Article
- Effects of neuronal nitric oxide synthase inhibition on microvascular and contractile function in skeletal muscle of aged rats.American journal of physiology. Heart and circulatory physiology · 2012Article
- Effects of chronic heart failure on neuronal nitric oxide synthase-mediated control of microvascular O2 pressure in contracting rat skeletal muscle.The Journal of physiology · 2012Article
- Effects of neuronal nitric oxide synthase inhibition on resting and exercising hindlimb muscle blood flow in the rat.The Journal of physiology · 2010Article
- Nitric oxide originating from NOS1 controls oxygen utilization and electrolyte transport efficiency in the diabetic kidney.American journal of physiology. Renal physiology · 2010Article
- Effects of chronic nitric oxide synthase inhibition on the cardiovascular responses to cannabinoids in vivo and in vitro.British journal of pharmacology · 2007Article
- Regional heterogeneity in the haemodynamic responses to urotensin II infusion in relation to UT receptor localisation.British journal of pharmacology · 2006Article
- Bolus injection of human UII in conscious rats evokes a biphasic haemodynamic response.British journal of pharmacology · 2004Article
- Comparative regional haemodynamic effects of the nitric oxide synthase inhibitors, S-methyl-L-thiocitrulline and L-NAME, in conscious rats.British journal of pharmacology · 2003Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. The regional haemodynamic effects of the putative nNOS inhibitor, S-methyl-L-thiocitrulline (SMTC), were compared with those of the nonselective NOS inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), in conscious, male Sprague-Dawley rats. 2. SMTC (0.3 mg kg(-1) bolus) produced a significant, short-lived, pressor effect associated with renal, mesenteric and hindquarters vasoconstriction; the same dose of L-NAME did not affect mean blood pressure (BP), although it caused bradycardia and mesenteric vasoconstriction. 3. At the highest dose tested (10 mg kg(-1)), L-NAME produced a significantly greater bradycardia and fall in mesenteric vascular conductance than SMTC, although the initial pressor response to SMTC was greater, but less sustained, than that to L-NAME. 4. Infusion of SMTC or L-NAME (3 mg kg(-1) h(-1)) induced rises in BP and falls in renal, mesenteric and hindquarters vascular conductances, but the effects of L-NAME were greater than those of SMTC, and L-NAME also caused bradycardia. 5. The renal vasodilator response to acetylcholine was markedly attenuated by infusion of L-NAME, but unaffected by SMTC. The hindquarters vasodilatation induced by salbutamol was attenuated by L-NAME, but not by SMTC. The mesenteric vasodilator response to bradykinin was modestly enhanced by SMTC, but not by L-NAME. The depressor and renal, mesenteric and hindquarters vasodilator responses to sodium nitroprusside were enhanced by L-NAME, whereas SMTC modestly enhanced the hypotensive and renal vasodilator effects of sodium nitroprusside, but attenuated the accompanying tachycardia. 6. The results are consistent with the cardiovascular effects of low doses of SMTC being attributable to nNOS inhibition.
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