| Adenine nucleotide control of coronary blood flow during exercise. | |
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MedLine Citation:
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PMID: 20852039 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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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:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural Date: 2010-09-17 |
Journal Detail:
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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:
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Created Date: 2010-12-03 Completed Date: 2011-01-13 Revised Date: 2011-12-21 |
Medline Journal Info:
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Nlm Unique ID: 100901228 Medline TA: Am J Physiol Heart Circ Physiol Country: United States |
Other Details:
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Languages: eng Pagination: H1981-9 Citation Subset: IM |
Affiliation:
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Department of Physiology and Biophysics, University of Washington, Seattle, Washington 98195-7290, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adenine Nucleotides
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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:
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R01 HL 82781/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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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 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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