Document Detail


K+ATP channels and adenosine are not necessary for coronary autoregulation.
MedLine Citation:
PMID:  9321819     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Autoregulation is defined as the intrinsic ability of an organ to maintain constant flow in the face of changing perfusion pressure. The present study evaluated the role of several potential mediators of coronary autoregulation: interstitial adenosine, ATP-sensitive K+ (K+ATP) channels, and myocardial oxygen and carbon dioxide tensions as reflected by coronary venous oxygen and carbon dioxide tensions. The left main coronary artery was cannulated, and blood was perfused at controlled pressures in closed-chest dogs. Interstitial adenosine concentration was estimated from arterial and venous adenosine concentrations with a previously described mathematical model. Autoregulation of coronary blood flow was observed between 100 and 60 mmHg. Glibenclamide, an inhibitor of K+ATP channels, reduced coronary blood flow by 19% at each perfusion pressure, but autoregulation was preserved. After stepwise reductions in coronary pressure to values > or = 70 mmHg, adenosine concentrations did not increase above basal levels. Adenosine concentration was elevated at 60 mmHg, suggesting a role for adenosine at the limit of coronary autoregulation. Adenosine is not required because glibenclamide, an inhibitor of adenosine-mediated vasodilation, did not reduce autoregulation or increase adenosine concentration. Coronary venous oxygen and carbon dioxide tensions were little changed during autoregulation before the inhibition of K+ATP channels and adenosine vasodilation with glibenclamide. However, coronary venous carbon dioxide tension rose progressively with decreasing coronary pressure after glibenclamide. The increase in carbon dioxide indirectly suggests that carbon dioxide-mediated vasodilation compensated for the loss of K+ATP-channel function. In summary, neither K+ATP channels nor adenosine is necessary to maintain coronary flow in the autoregulatory range of coronary arterial pressure from 100 to 60 mmHg.
Authors:
D W Stepp; K Kroll; E O Feigl
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The American journal of physiology     Volume:  273     ISSN:  0002-9513     ISO Abbreviation:  Am. J. Physiol.     Publication Date:  1997 Sep 
Date Detail:
Created Date:  1997-10-23     Completed Date:  1997-10-23     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0370511     Medline TA:  Am J Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  H1299-308     Citation Subset:  IM    
Affiliation:
Department of Physiology and Biophysics, University of Washington, Seattle 98195-7290, USA.
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MeSH Terms
Descriptor/Qualifier:
ATP-Binding Cassette Transporters
Adenosine / blood,  physiology*
Animals
Blood Pressure
Carbon Dioxide / blood
Coronary Circulation / drug effects,  physiology*
Dogs
Extracellular Space / physiology
Glyburide / pharmacology
Heart / physiology*
Heart Rate
Hemodynamics / drug effects,  physiology*
Homeostasis
Male
Models, Cardiovascular
Myocardium / metabolism
Oxygen / blood
Oxygen Consumption
Partial Pressure
Potassium Channels / physiology*
Potassium Channels, Inwardly Rectifying
Regional Blood Flow
Grant Support
ID/Acronym/Agency:
HL-07403/HL/NHLBI NIH HHS; HL-49822/HL/NHLBI NIH HHS; RR-01234/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/ATP-Binding Cassette Transporters; 0/Potassium Channels; 0/Potassium Channels, Inwardly Rectifying; 0/uK-ATP-1 potassium channel; 10238-21-8/Glyburide; 124-38-9/Carbon Dioxide; 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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