Document Detail

Effects of inhibition of nitric oxide formation on basal vasomotion and endothelium-dependent responses of the coronary arteries in awake dogs.
MedLine Citation:
PMID:  2040689     Owner:  NLM     Status:  MEDLINE    
The role of nitric oxide in basal vasomotor tone and stimulated endothelium-dependent dilations in the coronary arteries in chronically instrumented awake dogs was studied by examining the consequences of inhibiting endogenous nitric oxide formation with the specific inhibitor of nitric oxide formation, NG-monomethyl-L-arginine (L-NMMA). In four awake dogs, coronary dimension crystals were chronically implanted on the circumflex artery for the measurement of epicardial coronary diameter, and Doppler flow probes were implanted for quantitation of phasic coronary blood flow (vasomotion of distal regulatory resistance vessels). Basal epicardial coronary diameter, acetylcholine-stimulated endothelium-dependent dilation, and flow-induced endothelium-dependent dilation of the epicardial arteries and phasic blood flow were recorded before, and after 5, 15, 50, and 120 mg/kg of L-NMMA. L-NMMA induced a dose-related increase in basal epicardial coronary vasomotor tone. There was an accompanying increase in aortic pressure and a decrease in heart rate. At doses greater than or equal to 50 mg/kg, rest phasic coronary blood flow was also decreased. Left ventricular end-diastolic pressure and contractility were not significantly changed. In contrast, the flow-induced or acetylcholine-stimulated endothelium-dependent responses were attenuated only after infusion of the highest does of L-NMMA (120 mg/kg). The changes in the basal vasomotor tone and acetylcholine-stimulated endothelium-dependent responses returned towards the control states in the presence of L-arginine (660 mg/kg). These data support the view that nitric oxide plays a significant role in modulating basal vasomotion and endothelial-dependent dilation stimulated by acetylcholine or increase in blood flow in epicardial coronary arteries and also influence the regulation of coronary blood flow during physiologic conditions.
A Chu; D E Chambers; C C Lin; W D Kuehl; R M Palmer; S Moncada; F R Cobb
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of clinical investigation     Volume:  87     ISSN:  0021-9738     ISO Abbreviation:  J. Clin. Invest.     Publication Date:  1991 Jun 
Date Detail:
Created Date:  1991-07-10     Completed Date:  1991-07-10     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  7802877     Medline TA:  J Clin Invest     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1964-8     Citation Subset:  AIM; IM    
Department of Medicine, Duke Medical Center, Durham, North Carolina.
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MeSH Terms
Acetylcholine / pharmacology
Arginine / analogs & derivatives,  pharmacology
Coronary Circulation / drug effects
Coronary Vessels / physiology*
Dose-Response Relationship, Drug
Endothelium, Vascular / physiology*
Hemodynamics / drug effects
Nitric Oxide / metabolism*
Regional Blood Flow
Vasomotor System / physiology*
Grant Support
Reg. No./Substance:
10102-43-9/Nitric Oxide; 17035-90-4/omega-N-Methylarginine; 51-84-3/Acetylcholine; 74-79-3/Arginine

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

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