Document Detail


Nitric oxide modulates coronary autoregulation in the guinea pig.
MedLine Citation:
PMID:  1374299     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
A guinea pig heart Langendorff preparation was used in the present study to test the hypothesis that the coronary endothelium modulates coronary autoregulation through the production of nitric oxide (NO). Pacing at 250 beats per minute and venting the left ventricle to ensure that the hearts did no external work were performed in an attempt to reduce the metabolic stimulus to coronary vasomotion and keep it constant. We measured the responses of coronary flow and oxygen metabolism to stepwise changes of the perfusion pressure over the range between 18 and 85 mm Hg. The hearts exhibited autoregulation between 25 and 55 mm Hg and active vasodilation at perfusion pressures above that range. Perfusion with 100 microM NG-nitro-L-arginine (NNLA), an inhibitor of NO synthase, decreased coronary flow over the entire range of perfusion pressures and abolished active vasodilation over 65 mm Hg, thus widening the autoregulatory range. The administration of 200 microM L-arginine, but not D-arginine, reversed the action of NNLA. Inhibition of the cyclooxygenase pathway by 10 microM indomethacin did not affect autoregulation. Perfusion with 1 nM arginine vasopressin, a direct smooth muscle constrictor, lowered coronary flow rate to the same extent as NNLA at 55 mm Hg but did not prevent the pressure-dependent increase in flow above that pressure. These observations suggest that 1) the coronary endothelium actively modulates coronary autoregulation through the production of NO but not prostanoids, 2) mechanical stress (shear stress and/or stretching secondary to vasodilation) may be the stimulus to NO production, especially above the autoregulatory range, and 3) autoregulatory tone is likely to be myogenic in origin rather than mediated by extrinsic vasoconstrictors.
Authors:
M Ueeda; S K Silvia; R A Olsson
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Publication Detail:
Type:  Comparative Study; In Vitro; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Circulation research     Volume:  70     ISSN:  0009-7330     ISO Abbreviation:  Circ. Res.     Publication Date:  1992 Jun 
Date Detail:
Created Date:  1992-06-11     Completed Date:  1992-06-11     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0047103     Medline TA:  Circ Res     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1296-303     Citation Subset:  IM    
Affiliation:
Department of Internal Medicine, University of South Florida, Tampa.
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MeSH Terms
Descriptor/Qualifier:
Amino Acid Oxidoreductases / antagonists & inhibitors
Animals
Coronary Circulation*
Coronary Vessels / physiology
Cyclooxygenase Inhibitors / pharmacology
Endothelium, Vascular / physiology
Guinea Pigs
Homeostasis*
Indomethacin / pharmacology
Myocardium / metabolism
Nitric Oxide*
Nitric Oxide Synthase
Oxygen Consumption
Perfusion
Vasopressins / pharmacology
Grant Support
ID/Acronym/Agency:
HL-30391/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Cyclooxygenase Inhibitors; 10102-43-9/Nitric Oxide; 11000-17-2/Vasopressins; 53-86-1/Indomethacin; EC 1.14.13.39/Nitric Oxide Synthase; EC 1.4.-/Amino Acid Oxidoreductases

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


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