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Article: Anoxic contractions in isolated canine cerebral arteries: Contribution of endothelium-derived factors, metabolites of arachidonic acid, and calcium entry

TitleAnoxic contractions in isolated canine cerebral arteries: Contribution of endothelium-derived factors, metabolites of arachidonic acid, and calcium entry
Authors
Issue Date1986
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/
Citation
Journal Of Cardiovascular Pharmacology, 1986, v. 8 SUPPL.8, p. S97-S101 How to Cite?
AbstractExperiments were designed to determine the role of the endothelial cells and the metabolism of arachidonic acid in anoxic contractions of isolated canine basilar arteries. Rings, with and without endothelium, of these arteries were suspended for isometric tension recording; anoxia was induced by switching the mixture gassing the organ chamber from 95% O2-5% CO2 to 95% N2-5% CO2. In rings with endothelium, anoxia evoked increases in tension under basal conditions and during contractions to 5-hydroxytryptamine, uridine triphosphate, prostaglandin F(2α), and high K+. Under control conditions, these anoxic contractions were not prevented by α-adrenergic and serotonergic antagonists, by apyrase, or by inhibitors of cyclooxygenase. Anoxia prevented endothelium-dependent relaxations evoked by vasopressin and thrombin. In rings without endothelium, anoxia caused increases in tension during contractions evoked by various agonists, and in unstimulated preparations after inhibition of cyclooxygenase. Anoxic contractions were abolished by calcium entry blockers. These observations suggest that anoxic contractions of isolated canine basilar artery can be explained by the release of endothelium-derived contracting factor(s) and the accelerated entry of calcium in the smooth muscle cells, which possibly results from a diversion of arachidonic acid from the cyclooxygenase to the lipoxygenase pathway.
Persistent Identifierhttp://hdl.handle.net/10722/170824
ISSN
2015 Impact Factor: 2.462
2015 SCImago Journal Rankings: 0.962
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorKatusic, ZSen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:11:01Z-
dc.date.available2012-10-30T06:11:01Z-
dc.date.issued1986en_US
dc.identifier.citationJournal Of Cardiovascular Pharmacology, 1986, v. 8 SUPPL.8, p. S97-S101en_US
dc.identifier.issn0160-2446en_US
dc.identifier.urihttp://hdl.handle.net/10722/170824-
dc.description.abstractExperiments were designed to determine the role of the endothelial cells and the metabolism of arachidonic acid in anoxic contractions of isolated canine basilar arteries. Rings, with and without endothelium, of these arteries were suspended for isometric tension recording; anoxia was induced by switching the mixture gassing the organ chamber from 95% O2-5% CO2 to 95% N2-5% CO2. In rings with endothelium, anoxia evoked increases in tension under basal conditions and during contractions to 5-hydroxytryptamine, uridine triphosphate, prostaglandin F(2α), and high K+. Under control conditions, these anoxic contractions were not prevented by α-adrenergic and serotonergic antagonists, by apyrase, or by inhibitors of cyclooxygenase. Anoxia prevented endothelium-dependent relaxations evoked by vasopressin and thrombin. In rings without endothelium, anoxia caused increases in tension during contractions evoked by various agonists, and in unstimulated preparations after inhibition of cyclooxygenase. Anoxic contractions were abolished by calcium entry blockers. These observations suggest that anoxic contractions of isolated canine basilar artery can be explained by the release of endothelium-derived contracting factor(s) and the accelerated entry of calcium in the smooth muscle cells, which possibly results from a diversion of arachidonic acid from the cyclooxygenase to the lipoxygenase pathway.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.meshArachidonic Aciden_US
dc.subject.meshArachidonic Acids - Metabolismen_US
dc.subject.meshCalcium - Metabolismen_US
dc.subject.meshCerebral Arteries - Physiopathologyen_US
dc.subject.meshCyclooxygenase Inhibitorsen_US
dc.subject.meshDiltiazem - Pharmacologyen_US
dc.subject.meshDinoprosten_US
dc.subject.meshDogsen_US
dc.subject.meshEndothelium - Analysisen_US
dc.subject.meshFemaleen_US
dc.subject.meshMaleen_US
dc.subject.meshPotassium - Pharmacologyen_US
dc.subject.meshProstaglandins F - Pharmacologyen_US
dc.subject.meshSerotonin - Pharmacologyen_US
dc.subject.meshUridine Triphosphate - Pharmacologyen_US
dc.subject.meshVasoconstrictionen_US
dc.titleAnoxic contractions in isolated canine cerebral arteries: Contribution of endothelium-derived factors, metabolites of arachidonic acid, and calcium entryen_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.doi10.1097/00005344-198600088-00020-
dc.identifier.pmid2433536-
dc.identifier.scopuseid_2-s2.0-0022843938en_US
dc.identifier.volume8en_US
dc.identifier.issueSUPPL.8en_US
dc.identifier.spageS97en_US
dc.identifier.epageS101en_US
dc.identifier.isiWOS:A1986F518100020-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridKatusic, ZS=7006971465en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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