Document Detail


ET-A receptor activity restrains coronary blood flow in the failing heart.
MedLine Citation:
PMID:  15167269     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Mingxiao Hou; YingJie Chen; Jay H Traverse; Yunfang Li; Michel Barsoum; Robert J Bache
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of cardiovascular pharmacology     Volume:  43     ISSN:  0160-2446     ISO Abbreviation:  J. Cardiovasc. Pharmacol.     Publication Date:  2004 Jun 
Date Detail:
Created Date:  2004-05-28     Completed Date:  2004-09-09     Revised Date:  2011-04-20    
Medline Journal Info:
Nlm Unique ID:  7902492     Medline TA:  J Cardiovasc Pharmacol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  764-9     Citation Subset:  IM    
Affiliation:
Department of Medicine, University of Minnesota Health Sciences Center, Minneapolis, USA.
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MeSH Terms
Descriptor/Qualifier:
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:
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:
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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