Document Detail

Effects of neuronal nitric oxide synthase inhibition on resting and exercising hindlimb muscle blood flow in the rat.
MedLine Citation:
PMID:  20176629     Owner:  NLM     Status:  MEDLINE    
Nitric oxide (NO) derived from endothelial NO synthase (eNOS) is an integral mediator of vascular control during muscle contractions. However, it is not known whether neuronal NOS (nNOS)-derived NO regulates tissue hyperaemia in healthy subjects, particularly during exercise. We tested the hypothesis that selective nNOS inhibition would reduce blood flow and vascular conductance (VC) in rat hindlimb locomotor muscle(s), kidneys and splanchnic organs at rest and during dynamic treadmill exercise (20 m min(-1), 10% grade). Nineteen male Sprague-Dawley rats (555 +/- 23 g) were assigned to either rest (n = 9) or exercise (n = 10) groups. Blood flow and VC were determined via radiolabelled microspheres before and after the intra-arterial administration of the selective nNOS inhibitor S-methyl-L-thiocitrulline (SMTC, 2.1 +/- 0.1 micromol kg(-1)). Total hindlimb muscle blood flow (control: 20 +/- 2 ml min(-1) 100g(-1), SMTC: 12 +/- 2 ml min(-1) 100g(-1), P < 0.05) and VC (control: 0.16 +/- 0.02 ml min(-1) 100 g(-1) mmHg(1), SMTC: 0.09 +/- 0.01 ml min(-1) 100 g(-1) mmHg(-1), P < 0.05) were reduced substantially at rest. Moreover, the magnitude of the absolute reduction in blood flow and VC correlated (P < 0.05) with the proportion of oxidative muscle fibres found in the individual muscles or muscle parts of the hindlimb. During exercise, total hindlimb blood flow (control: 108 +/- 7 ml min(-1) 100 g(-1), SMTC: 105 +/- 8 ml min(-1) 100 g(-1)) and VC (control: 0.77 +/- 0.06 ml min(-1) 100g(-1) mmHg(-1); SMTC: 0.70 +/- 0.05 ml min(-1) 100g(-1) mmHg(-1)) were not different (P > 0.05) between control and SMTC conditions. SMTC reduced (P < 0.05) blood flow and VC at rest and during exercise in the kidneys, adrenals and liver. These results enhance our understanding of the role of NO-mediated circulatory control by demonstrating that nNOS does not appear to subserve an obligatory role in the exercising muscle hyperaemic response in the rat.
Steven W Copp; Daniel M Hirai; Peter J Schwagerl; Timothy I Musch; David C Poole
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-02-22
Journal Detail:
Title:  The Journal of physiology     Volume:  588     ISSN:  1469-7793     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2010 Apr 
Date Detail:
Created Date:  2010-04-16     Completed Date:  2010-07-29     Revised Date:  2013-05-30    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  1321-31     Citation Subset:  IM    
Department of Kinesiology, Kansas State University, Manhattan, KS 66506-5802, USA.
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MeSH Terms
Blood Pressure / drug effects
Citrulline / analogs & derivatives,  pharmacology
Enzyme Inhibitors / pharmacology
Heart Rate / drug effects
Hindlimb / blood supply*
Models, Animal
Muscle Contraction / physiology
Muscle, Skeletal / blood supply*
NG-Nitroarginine Methyl Ester / pharmacology
Nitric Oxide Synthase Type I / antagonists & inhibitors*,  drug effects,  metabolism
Physical Conditioning, Animal / physiology*
Rats, Sprague-Dawley
Regional Blood Flow / drug effects,  physiology*
Rest / physiology*
Thiourea / analogs & derivatives,  pharmacology
Reg. No./Substance:
0/Enzyme Inhibitors; 156719-41-4/S-methylthiocitrulline; 372-75-8/Citrulline; 50903-99-6/NG-Nitroarginine Methyl Ester; 62-56-6/Thiourea; EC Oxide Synthase Type I

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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