| Effect of K+ATP channel and adenosine receptor blockade during rest and exercise in congestive heart failure. | |
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MedLine Citation:
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PMID: 17478726 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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K(+)(ATP) channels are important metabolic regulators of coronary blood flow (CBF) that are activated in the setting of reduced levels of ATP or perfusion pressure. In the normal heart, blockade of K(+)(ATP) channels results in a approximately 20% reduction in resting CBF but does not impair the increase in CBF that occurs during exercise. In contrast, adenosine receptor blockade fails to alter CBF or myocardial oxygen consumption (MVO(2)) in the normal heart but contributes to the increase in CBF during exercise when vascular K(+)(ATP) channels are blocked. Congestive heart failure (CHF) is associated with a decrease in CBF that is matched to a decrease in MVO(2) suggesting downregulation of myocardial energy utilization. Because myocardial ATP levels and coronary perfusion pressure are reduced in CHF, this study was undertaken to examine the role of K(+)(ATP) channels and adenosine in dogs with pacing-induced CHF. Myocardial blood flow (MBF) and MVO(2) were measured during rest and treadmill exercise before and after K(+)(ATP) channel blockade with glibenclamide (50 microg/kg/min ic) or adenosine receptor blockade with 8-phenyltheophylline (8-PT; 5 mg/kg iv). Inhibition of K(+)(ATP) channels resulted in a decrease in CBF and MVO(2) at rest and during exercise without a change in the relationship between CBF and MVO(2). In contrast, adenosine receptor blockade caused a significant increase in CBF that occurred secondary to an increase of MVO(2). These findings demonstrate that coronary K(+)(ATP) channel activity contribute to the regulation of resting MBF in CHF, and that endogenous adenosine may act to inhibit MVO(2) in the failing heart. |
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Authors:
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Jay H Traverse; YingJie Chen; MingXiao Hou; Yunfang Li; Robert J Bache |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2007-05-03 |
Journal Detail:
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Title: Circulation research Volume: 100 ISSN: 1524-4571 ISO Abbreviation: Circ. Res. Publication Date: 2007 Jun |
Date Detail:
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Created Date: 2007-06-08 Completed Date: 2007-06-19 Revised Date: 2011-04-20 |
Medline Journal Info:
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Nlm Unique ID: 0047103 Medline TA: Circ Res Country: United States |
Other Details:
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Languages: eng Pagination: 1643-9 Citation Subset: IM |
Affiliation:
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Department of Medicine, University of Minnesota Medical School, Minneapolis, MN 55455, USA. trave004@umn.edu |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adenosine Triphosphate
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metabolism Animals Anti-Arrhythmia Agents / pharmacology Blood Flow Velocity / drug effects Cardiac Pacing, Artificial Coronary Circulation / drug effects Disease Models, Animal Dogs Exercise Test Glyburide / pharmacology Heart / drug effects, physiopathology* Heart Failure / physiopathology* Oxygen Consumption / drug effects Physical Exertion* / drug effects Pinacidil / pharmacology Potassium Channel Blockers / pharmacology* Potassium Channels / drug effects*, metabolism Purinergic P1 Receptor Antagonists* Rest Theophylline / analogs & derivatives, pharmacology Vasodilator Agents / pharmacology |
| Grant Support | |
ID/Acronym/Agency:
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HL20598/HL/NHLBI NIH HHS; HL21872/HL/NHLBI NIH HHS; HL71790/HL/NHLBI NIH HHS; R01 HL071790-01A1/HL/NHLBI NIH HHS; R01 HL071790-02/HL/NHLBI NIH HHS; R01 HL071790-03/HL/NHLBI NIH HHS; R01 HL071790-04/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Anti-Arrhythmia Agents; 0/Potassium Channel Blockers; 0/Potassium Channels; 0/Purinergic P1 Receptor Antagonists; 0/Vasodilator Agents; 10238-21-8/Glyburide; 56-65-5/Adenosine Triphosphate; 58-55-9/Theophylline; 85371-64-8/Pinacidil; 961-45-5/8-phenyltheophylline |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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