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Article: Does endothelin-1 mediate endothelium-dependent contractions during anoxia?

TitleDoes endothelin-1 mediate endothelium-dependent contractions during anoxia?
Authors
Issue Date1989
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/
Citation
Journal Of Cardiovascular Pharmacology, 1989, v. 13 SUPPL. 5, p. S124-S128 How to Cite?
AbstractEndothelin-1 (ET-1) is a more potent constrictor of femoral venous than femoral arterial smooth muscle. By contrast, endothelium-dependent contractions to anoxia are more prominent in the artery. Unlike those to ET-1, the endothelium-dependent contractions evoked by anoxia are rapid in onset and readily reversible; they are antagonized by Ca2+ entry blockers. ET-1-induced responses are inhibited by endothelium-dependent relaxing factors in canine arteries, and to a lower extent in veins. ET-1 does not augment the production of cyclic GMP in cultured porcine aortic endothelial cells, or in canine arteries and veins, suggesting that the peptide does not evoke the release of endothelium-dependent relaxing factor (EDRF) in canine blood vessels. The endothelium-derived contracting factor (EDCF) released during anoxic contraction cannot be bioassayed, under conditions where ET-1 causes contraction of the bioassay tissue. No ET-1 appears to be released in the extracellular space during anoxic contractions. These findings do not support the hypothesis that ET-1 is the EDCF released by anoxia.
Persistent Identifierhttp://hdl.handle.net/10722/170951
ISSN
2015 Impact Factor: 2.462
2015 SCImago Journal Rankings: 0.962
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorAuchSchwelk, Wen_US
dc.contributor.authorBoulanger, Cen_US
dc.contributor.authorJanssen, PAen_US
dc.contributor.authorKatusic, ZSen_US
dc.contributor.authorKomori, Ken_US
dc.contributor.authorMiller, VMen_US
dc.contributor.authorSchini, VBen_US
dc.contributor.authorVidal, Men_US
dc.date.accessioned2012-10-30T06:11:35Z-
dc.date.available2012-10-30T06:11:35Z-
dc.date.issued1989en_US
dc.identifier.citationJournal Of Cardiovascular Pharmacology, 1989, v. 13 SUPPL. 5, p. S124-S128en_US
dc.identifier.issn0160-2446en_US
dc.identifier.urihttp://hdl.handle.net/10722/170951-
dc.description.abstractEndothelin-1 (ET-1) is a more potent constrictor of femoral venous than femoral arterial smooth muscle. By contrast, endothelium-dependent contractions to anoxia are more prominent in the artery. Unlike those to ET-1, the endothelium-dependent contractions evoked by anoxia are rapid in onset and readily reversible; they are antagonized by Ca2+ entry blockers. ET-1-induced responses are inhibited by endothelium-dependent relaxing factors in canine arteries, and to a lower extent in veins. ET-1 does not augment the production of cyclic GMP in cultured porcine aortic endothelial cells, or in canine arteries and veins, suggesting that the peptide does not evoke the release of endothelium-dependent relaxing factor (EDRF) in canine blood vessels. The endothelium-derived contracting factor (EDCF) released during anoxic contraction cannot be bioassayed, under conditions where ET-1 causes contraction of the bioassay tissue. No ET-1 appears to be released in the extracellular space during anoxic contractions. These findings do not support the hypothesis that ET-1 is the EDCF released by anoxia.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.subject.meshAnimalsen_US
dc.subject.meshAnoxia - Physiopathologyen_US
dc.subject.meshEndothelinsen_US
dc.subject.meshEndothelium, Vascular - Drug Effectsen_US
dc.subject.meshMuscle Contraction - Drug Effectsen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effectsen_US
dc.subject.meshPeptides - Pharmacologyen_US
dc.titleDoes endothelin-1 mediate endothelium-dependent contractions during anoxia?en_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1097/00005344-198900135-00031-
dc.identifier.pmid2473285-
dc.identifier.scopuseid_2-s2.0-0024506465en_US
dc.identifier.volume13en_US
dc.identifier.issueSUPPL. 5en_US
dc.identifier.spageS124en_US
dc.identifier.epageS128en_US
dc.identifier.isiWOS:A1989U406600025-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridAuchSchwelk, W=7003395589en_US
dc.identifier.scopusauthoridBoulanger, C=7006599024en_US
dc.identifier.scopusauthoridJanssen, PA=36042383000en_US
dc.identifier.scopusauthoridKatusic, ZS=7006971465en_US
dc.identifier.scopusauthoridKomori, K=8977740100en_US
dc.identifier.scopusauthoridMiller, VM=7201476816en_US
dc.identifier.scopusauthoridSchini, VB=7004113565en_US
dc.identifier.scopusauthoridVidal, M=7202764932en_US

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