| ET-A receptor activity restrains coronary blood flow in the failing heart. | |
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MedLine Citation:
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PMID: 15167269 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Circulating levels of the potent vasoconstrictor peptide endothelin-1 (ET-1) are increased in congestive heart failure (CHF). Coronary blood flow and myocardial oxygen consumption (MVO2) are decreased in some models of CHF. This study tested the hypothesis that ET-1 induced coronary vasoconstriction limits oxygen availability in the failing heart. The effects of selective ET-A receptor blockade with BQ610 (5 microg/min, intracoronary) and selective ET-B receptor blockade with BQ788 (5 microg/min, intracoronary) on coronary blood flow were examined at rest and during graded treadmill exercise in 8 dogs in which congestive heart failure (CHF) had been produced by rapid ventricular pacing for three to four weeks. In animals with CHF, ET-B receptor blockade caused no change in left ventricular (LV) pressure or coronary blood flow. In contrast, ET-A blockade with BQ610 resulted in modest significant increases of coronary blood flow at rest (from 22.4 +/- 2.1 to 27.9 +/- 3.0 mL/min) and during two exercise stages (from 26.9 +/- 2.0 to 30.7 +/- 1.9 during stage 1 exercise and from 28.5 +/- 2.0 to 31.7 +/- 1.3 mL/min during stage 2; all P < 0.05), with an upward shift in the relationship between coronary flow and rate-pressure product. The increase in coronary flow produced by ET-A blockade was not associated with an increase of either myocardial oxygen uptake or LV dP/dt. Thus, although ET-A receptor blockade caused a modest increase in coronary flow, this did not result in an increase of MVO2, implying that ET-A-mediated coronary vasoconstriction did not limit oxygen uptake by the failing heart. |
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Authors:
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Mingxiao Hou; YingJie Chen; Jay H Traverse; Yunfang Li; Michel Barsoum; Robert J Bache |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Journal of cardiovascular pharmacology Volume: 43 ISSN: 0160-2446 ISO Abbreviation: J. Cardiovasc. Pharmacol. Publication Date: 2004 Jun |
Date Detail:
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Created Date: 2004-05-28 Completed Date: 2004-09-09 Revised Date: 2011-04-20 |
Medline Journal Info:
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Nlm Unique ID: 7902492 Medline TA: J Cardiovasc Pharmacol Country: United States |
Other Details:
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Languages: eng Pagination: 764-9 Citation Subset: IM |
Affiliation:
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Department of Medicine, University of Minnesota Health Sciences Center, Minneapolis, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Coronary Circulation / drug effects, physiology* Dogs Dose-Response Relationship, Drug Endothelin-1 / pharmacology Heart Failure / metabolism, physiopathology* Oligopeptides / pharmacology Receptor, Endothelin A / agonists, antagonists & inhibitors, physiology* |
| Grant Support | |
ID/Acronym/Agency:
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HL20598/HL/NHLBI NIH HHS; HL21872/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/Endothelin-1; 0/Oligopeptides; 0/Receptor, Endothelin A; 141595-53-1/BQ 610 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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