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Article: Hypoxia releases a vasoconstrictor substance from the canine vascular endothelium

TitleHypoxia releases a vasoconstrictor substance from the canine vascular endothelium
Authors
Issue Date1985
PublisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0022-3751
Citation
Journal Of Physiology, 1985, v. VOL. 364, p. 45-56 How to Cite?
Abstract1. Experiments were designed to determine the role of the endothelium in the facilitation by anoxia of contractile responses of isolated coronary arteries. 2. Rings and strips of canine coronary arteries, with or without endothelium, were suspended for isometric tension recording in modified Krebs-Ringer bicarbonate solution. To determine the release of a vasoactive substance(s) from the endothelial cells, strips without endothelium were layered with strips containing endothelium. 3. In rings and in layered preparations with endothelium, anoxia (95% N2-5% CO2) augmented contractile responses to prostaglandin F(2α). Hypoxia (10 or 5% O2) caused contractions in the presence of indomethacin. Removal of the endothelium abolished the anoxic facilitation, and the hypoxic contractions. 4. Inhibitors of cyclo-oxygenase, lipoxygenase or phospholipase A2 or of adrenergic, serotonergic and histaminergic receptors did not prevent the response to anoxia. Likewise, inhibitors of the endothelium-derived factor(s) (quinacrine, phenidone and methylene blue) did not affect the anoxic facilitation. 5. Hypoxia and anoxia caused contraction of coronary arteries without endothelium when layered with femoral arteries and veins with endothelium. Anoxic facilitation was observed in femoral arteries, but not in femoral veins, with endothelium. 6. These experiments indicate that hypoxia and anoxia cause the release of a diffusible vasoconstrictor substance(s) from endothelial cells. The sensitivity of smooth muscle of different anatomical origin to the facilitatory mediator(s) varies.
Persistent Identifierhttp://hdl.handle.net/10722/170771
ISSN
2015 Impact Factor: 4.731
2015 SCImago Journal Rankings: 2.670
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorRubanyi, GMen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:10:47Z-
dc.date.available2012-10-30T06:10:47Z-
dc.date.issued1985en_US
dc.identifier.citationJournal Of Physiology, 1985, v. VOL. 364, p. 45-56en_US
dc.identifier.issn0022-3751en_US
dc.identifier.urihttp://hdl.handle.net/10722/170771-
dc.description.abstract1. Experiments were designed to determine the role of the endothelium in the facilitation by anoxia of contractile responses of isolated coronary arteries. 2. Rings and strips of canine coronary arteries, with or without endothelium, were suspended for isometric tension recording in modified Krebs-Ringer bicarbonate solution. To determine the release of a vasoactive substance(s) from the endothelial cells, strips without endothelium were layered with strips containing endothelium. 3. In rings and in layered preparations with endothelium, anoxia (95% N2-5% CO2) augmented contractile responses to prostaglandin F(2α). Hypoxia (10 or 5% O2) caused contractions in the presence of indomethacin. Removal of the endothelium abolished the anoxic facilitation, and the hypoxic contractions. 4. Inhibitors of cyclo-oxygenase, lipoxygenase or phospholipase A2 or of adrenergic, serotonergic and histaminergic receptors did not prevent the response to anoxia. Likewise, inhibitors of the endothelium-derived factor(s) (quinacrine, phenidone and methylene blue) did not affect the anoxic facilitation. 5. Hypoxia and anoxia caused contraction of coronary arteries without endothelium when layered with femoral arteries and veins with endothelium. Anoxic facilitation was observed in femoral arteries, but not in femoral veins, with endothelium. 6. These experiments indicate that hypoxia and anoxia cause the release of a diffusible vasoconstrictor substance(s) from endothelial cells. The sensitivity of smooth muscle of different anatomical origin to the facilitatory mediator(s) varies.en_US
dc.languageengen_US
dc.publisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0022-3751en_US
dc.relation.ispartofJournal of Physiologyen_US
dc.subject.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAdenosine Diphosphate - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCoronary Vessels - Physiologyen_US
dc.subject.meshDinoprosten_US
dc.subject.meshDogsen_US
dc.subject.meshEndothelium - Physiologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshIndomethacin - Pharmacologyen_US
dc.subject.meshIsometric Contractionen_US
dc.subject.meshMaleen_US
dc.subject.meshMethylene Blue - Pharmacologyen_US
dc.subject.meshMuscle, Smooth, Vascular - Physiologyen_US
dc.subject.meshOxygen - Physiologyen_US
dc.subject.meshProstaglandins F - Pharmacologyen_US
dc.subject.meshPyrazoles - Pharmacologyen_US
dc.subject.meshQuinacrine - Pharmacologyen_US
dc.subject.meshVasoconstriction - Drug Effectsen_US
dc.titleHypoxia releases a vasoconstrictor substance from the canine vascular endotheliumen_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.pmid3861856-
dc.identifier.scopuseid_2-s2.0-0021891159en_US
dc.identifier.volumeVOL. 364en_US
dc.identifier.spage45en_US
dc.identifier.epage56en_US
dc.identifier.isiWOS:A1985AMT3300004-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridRubanyi, GM=7005517991en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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