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Conference Paper: The ET(A) antagonist BQ-123 inhibits anoxic contractions of canine coronary arteries without endothelium

TitleThe ET(A) antagonist BQ-123 inhibits anoxic contractions of canine coronary arteries without endothelium
Authors
KeywordsAnoxic contraction
Coronary artery
Endothelin
Vascular smooth muscle
Issue Date1993
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/
Citation
Journal Of Cardiovascular Pharmacology, 1993, v. 22 SUPPL. 8, p. S252-S256 How to Cite?
AbstractExperiments were designed to determine whether or not endogenous endothelin (ET) contributes to endothelium-independent anoxic contractions of canine coronary arteries. Rings without endothelium were suspended for isometric tension recording in conventional organ chambers filled with modified Krebs-Ringer bicarbonate solution. Anoxia (PO2 ≤1 mm Hg) caused reproducible contractions. The anoxic contractions were augmented by exogenous endothelin-1 (ET-1). At 10-6 M and 10-5 M, BQ-123 (a specific endothelin antagonist) inhibited both the facilitatory effect of ET-1 and the anoxic contractions. At these concentrations BQ-123 caused a parallel shift to the right of the concentration-response curve to ET-1 and a small but significant depression of the response to norepinephrine, without affecting the maximal response to the catecholamine. BQ-123 did not significantly affect the concentration-response curve to Ca2+ in depolarizing solution (60 mM KCl). Monoclonal antibodies against ET-1 (70 μg/ml) inhibited the response to exogenous ET-1 and abolished the facilitating effect of the peptide, but did not affect the anoxic contractions. These results suggest that ET-1 contributes to anoxic contractions in canine coronary arteries without endothelium. The receptor involved belongs to the ET(A)-subtype and is not accessible to monoclonal antibodies.
Persistent Identifierhttp://hdl.handle.net/10722/173517
ISSN
2023 Impact Factor: 2.6
2023 SCImago Journal Rankings: 0.610
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorVedernikov, YPen_US
dc.contributor.authorGoto, Ken_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:32:28Z-
dc.date.available2012-10-30T06:32:28Z-
dc.date.issued1993en_US
dc.identifier.citationJournal Of Cardiovascular Pharmacology, 1993, v. 22 SUPPL. 8, p. S252-S256en_US
dc.identifier.issn0160-2446en_US
dc.identifier.urihttp://hdl.handle.net/10722/173517-
dc.description.abstractExperiments were designed to determine whether or not endogenous endothelin (ET) contributes to endothelium-independent anoxic contractions of canine coronary arteries. Rings without endothelium were suspended for isometric tension recording in conventional organ chambers filled with modified Krebs-Ringer bicarbonate solution. Anoxia (PO2 ≤1 mm Hg) caused reproducible contractions. The anoxic contractions were augmented by exogenous endothelin-1 (ET-1). At 10-6 M and 10-5 M, BQ-123 (a specific endothelin antagonist) inhibited both the facilitatory effect of ET-1 and the anoxic contractions. At these concentrations BQ-123 caused a parallel shift to the right of the concentration-response curve to ET-1 and a small but significant depression of the response to norepinephrine, without affecting the maximal response to the catecholamine. BQ-123 did not significantly affect the concentration-response curve to Ca2+ in depolarizing solution (60 mM KCl). Monoclonal antibodies against ET-1 (70 μg/ml) inhibited the response to exogenous ET-1 and abolished the facilitating effect of the peptide, but did not affect the anoxic contractions. These results suggest that ET-1 contributes to anoxic contractions in canine coronary arteries without endothelium. The receptor involved belongs to the ET(A)-subtype and is not accessible to monoclonal antibodies.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/en_US
dc.relation.ispartofJournal of Cardiovascular Pharmacologyen_US
dc.subjectAnoxic contraction-
dc.subjectCoronary artery-
dc.subjectEndothelin-
dc.subjectVascular smooth muscle-
dc.subject.meshAnimalsen_US
dc.subject.meshAnoxia - Physiopathologyen_US
dc.subject.meshAntibodies, Monoclonal - Pharmacologyen_US
dc.subject.meshCoronary Vessels - Physiologyen_US
dc.subject.meshDogsen_US
dc.subject.meshEndothelins - Immunology - Pharmacologyen_US
dc.subject.meshEndothelium, Vascular - Physiologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshIsometric Contraction - Drug Effectsen_US
dc.subject.meshMaleen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effectsen_US
dc.subject.meshPeptides, Cyclic - Pharmacologyen_US
dc.subject.meshReceptors, Endothelin - Antagonists & Inhibitorsen_US
dc.titleThe ET(A) antagonist BQ-123 inhibits anoxic contractions of canine coronary arteries without endotheliumen_US
dc.typeConference_Paperen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1097/00005344-199322008-00067-
dc.identifier.pmid7509958en_US
dc.identifier.scopuseid_2-s2.0-0027739279en_US
dc.identifier.volume22en_US
dc.identifier.issueSUPPL. 8en_US
dc.identifier.spageS252en_US
dc.identifier.epageS256en_US
dc.identifier.isiWOS:A1993MN02800067-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridVedernikov, YP=35461855900en_US
dc.identifier.scopusauthoridGoto, K=16156562100en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.issnl0160-2446-

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