Document Detail


Role of nitric oxide and adenosine in control of coronary blood flow in exercising dogs.
MedLine Citation:
PMID:  10869267     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Inhibition of nitric oxide (NO) synthesis results in very little change in coronary blood flow, but this is thought to be because cardiac adenosine concentration increases to compensate for the loss of NO vasodilation. Accordingly, in the present study, adenosine measurements were made before and during NO synthesis inhibition during exercise. METHODS AND RESULTS: Experiments were performed in chronically instrumented dogs at rest and during graded treadmill exercise before and during inhibition of NO synthesis with N(omega)-nitro-L-arginine (L-NNA, 35 mg/kg IV). Before inhibition of NO synthesis, myocardial oxygen consumption increased approximately 3.7-fold, and coronary blood flow increased approximately 3.2-fold from rest to the highest level of exercise, and this was not changed by NO synthesis inhibition. Coronary venous oxygen tension was modestly reduced by L-NNA at all levels of myocardial oxygen consumption. However, the slope of the relationship between myocardial oxygen consumption and coronary venous oxygen tension was not altered by L-NNA. Inhibition of NO synthesis did not increase coronary venous plasma or estimated interstitial adenosine concentration. During exercise, estimated interstitial adenosine remained well below the threshold concentration necessary for coronary vasodilation before or after L-NNA. CONCLUSIONS: NO causes a modest coronary vasodilation at rest and during exercise but does not act as a local metabolic vasodilator. Adenosine does not mediate a compensatory local metabolic coronary vasodilation when NO synthesis is inhibited.
Authors:
J D Tune; K N Richmond; M W Gorman; E O Feigl
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Circulation     Volume:  101     ISSN:  1524-4539     ISO Abbreviation:  Circulation     Publication Date:  2000 Jun 
Date Detail:
Created Date:  2000-07-19     Completed Date:  2000-07-19     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  2942-8     Citation Subset:  AIM; IM    
Affiliation:
Department of Physiology and Biophysics, University of Washington School of Medicine, Seattle, WA 98195-7290, USA.
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MeSH Terms
Descriptor/Qualifier:
Adenosine / blood,  physiology*
Animals
Coronary Circulation / physiology*
Coronary Vessels
Dogs
Enzyme Inhibitors / pharmacology
Male
Motor Activity / physiology*
Myocardium / metabolism
Nitric Oxide / antagonists & inhibitors,  physiology*
Nitroarginine / pharmacology
Oxygen / blood
Oxygen Consumption
Veins
Grant Support
ID/Acronym/Agency:
HL49170/HL/NHLBI NIH HHS; HL49822/HL/NHLBI NIH HHS; RR01243/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Enzyme Inhibitors; 10102-43-9/Nitric Oxide; 2149-70-4/Nitroarginine; 58-61-7/Adenosine; 7782-44-7/Oxygen

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


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