Document Detail


Adenine nucleotide control of coronary blood flow during exercise.
MedLine Citation:
PMID:  20852039     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The adenine nucleotide hypothesis postulates that the ATP released from red blood cells is broken down to ADP and AMP in coronary capillaries and that ATP, ADP, and AMP act on purinergic receptors on the surface of capillary endothelial cells. Purinergic receptor activation initiates a retrograde conducted vasodilator signal to the upstream arteriole that controls coronary blood flow in a negative feedback manner. A previous study (M. Farias 3rd, M. W. Gorman, M. V. Savage, and E. O. Feigl, Am J Physiol Heart Circ Physiol 288: H1586-H1590, 2005) demonstrated that coronary venous plasma ATP concentration increased during exercise and correlated with coronary blood flow. The present experiments test the adenine nucleotide hypothesis by examining the balance between oxygen delivery (via coronary blood flow) and myocardial oxygen consumption during exercise before and after purinergic receptor blockade. Dogs (n = 7) were chronically instrumented with catheters in the aorta and coronary sinus and a flow transducer around the circumflex coronary artery. During control treadmill exercise, myocardial oxygen consumption increased and the balance between oxygen delivery and myocardial oxygen consumption fell as indicated by a declining coronary venous oxygen tension. Blockade of P1 and P2Y(1) purinergic receptors combined with inhibition of nitric oxide synthesis significantly decreased the balance between oxygen delivery and myocardial oxygen consumption compared with control. The results support the hypothesis that ATP and its breakdown products ADP and AMP are part of a negative feedback control mechanism that matches coronary blood flow to myocardial oxygen consumption at rest and during exercise.
Authors:
Mark W Gorman; G Alec Rooke; Margaret V Savage; M P Suresh Jayasekara; Kenneth A Jacobson; Eric O Feigl
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural     Date:  2010-09-17
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  299     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2010-12-03     Completed Date:  2011-01-13     Revised Date:  2013-05-27    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1981-9     Citation Subset:  IM    
Affiliation:
Department of Physiology and Biophysics, University of Washington, Seattle, Washington 98195-7290, USA.
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MeSH Terms
Descriptor/Qualifier:
Adenine Nucleotides / metabolism*
Adenosine Diphosphate / metabolism
Adenosine Monophosphate / metabolism
Adenosine Triphosphate / metabolism
Animals
Coronary Circulation* / drug effects
Coronary Vessels / drug effects,  metabolism*
Dogs
Enzyme Inhibitors / pharmacology
Feedback, Physiological
Male
Myocardium / metabolism*
Nitric Oxide / metabolism
Nitric Oxide Synthase / antagonists & inhibitors,  metabolism
Oxygen / blood
Oxygen Consumption
Physical Exertion*
Purinergic P1 Receptor Antagonists / pharmacology
Purinergic P2Y Receptor Antagonists / pharmacology
Receptors, Purinergic P1 / drug effects,  metabolism*
Receptors, Purinergic P2Y1 / drug effects,  metabolism*
Regional Blood Flow
Grant Support
ID/Acronym/Agency:
R01 HL 82781/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Adenine Nucleotides; 0/Enzyme Inhibitors; 0/Purinergic P1 Receptor Antagonists; 0/Purinergic P2Y Receptor Antagonists; 0/Receptors, Purinergic P1; 0/Receptors, Purinergic P2Y1; 10102-43-9/Nitric Oxide; 56-65-5/Adenosine Triphosphate; 58-64-0/Adenosine Diphosphate; 61-19-8/Adenosine Monophosphate; 7782-44-7/Oxygen; EC 1.14.13.39/Nitric Oxide Synthase
Comments/Corrections

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