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Article: Electrical and mechanical changes during anoxic contractions of the isolated canine basilar artery

TitleElectrical and mechanical changes during anoxic contractions of the isolated canine basilar artery
Authors
KeywordsAnoxia
Basilar artery
Ca2+
Channel
Channel inhibitors
Dependent Ca2+
Depolarization
Hyperpolarization
Voltage
Issue Date1993
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/jcbfm
Citation
Journal Of Cerebral Blood Flow And Metabolism, 1993, v. 13 n. 3, p. 498-502 How to Cite?
AbstractIsometric tension and membrane potential were measured to determine the electrophysiological events occurring during anoxia in the isolated canine basilar artery. Anoxia induced transient contractions which were inhibited by the Ca2+-channel inhibitor, diltiazem, and were abolished in Ca2+-free solution. Anoxic contractions were accompanied by membrane depolarizations, which were resistant to diltiazem. When matched contractions were obtained with anoxia and high K+, the level of membrane depolarization was smaller during anoxic contractions. These results support the importance of voltage- dependent Ca2+ influx in the generation of anoxic contractions in the canine basilar artery. However, membrane depolarization does not fully account for these anoxic contractions.
Persistent Identifierhttp://hdl.handle.net/10722/171090
ISSN
2021 Impact Factor: 6.960
2020 SCImago Journal Rankings: 2.167
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorNagao, Ten_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:09Z-
dc.date.available2012-10-30T06:12:09Z-
dc.date.issued1993en_US
dc.identifier.citationJournal Of Cerebral Blood Flow And Metabolism, 1993, v. 13 n. 3, p. 498-502en_US
dc.identifier.issn0271-678Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/171090-
dc.description.abstractIsometric tension and membrane potential were measured to determine the electrophysiological events occurring during anoxia in the isolated canine basilar artery. Anoxia induced transient contractions which were inhibited by the Ca2+-channel inhibitor, diltiazem, and were abolished in Ca2+-free solution. Anoxic contractions were accompanied by membrane depolarizations, which were resistant to diltiazem. When matched contractions were obtained with anoxia and high K+, the level of membrane depolarization was smaller during anoxic contractions. These results support the importance of voltage- dependent Ca2+ influx in the generation of anoxic contractions in the canine basilar artery. However, membrane depolarization does not fully account for these anoxic contractions.en_US
dc.languageengen_US
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/jcbfmen_US
dc.relation.ispartofJournal of Cerebral Blood Flow and Metabolismen_US
dc.subjectAnoxia-
dc.subjectBasilar artery-
dc.subjectCa2+-
dc.subjectChannel-
dc.subjectChannel inhibitors-
dc.subjectDependent Ca2+-
dc.subjectDepolarization-
dc.subjectHyperpolarization-
dc.subjectVoltage-
dc.subject.meshAnimalsen_US
dc.subject.meshAnoxia - Physiopathologyen_US
dc.subject.meshBasilar Artery - Drug Effects - Pathology - Physiopathologyen_US
dc.subject.meshCalcium - Pharmacologyen_US
dc.subject.meshDiltiazem - Pharmacologyen_US
dc.subject.meshDogsen_US
dc.subject.meshElectrophysiologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshMaleen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effects - Pathology - Physiopathologyen_US
dc.subject.meshPotassium - Pharmacologyen_US
dc.subject.meshVasoconstriction - Physiologyen_US
dc.titleElectrical and mechanical changes during anoxic contractions of the isolated canine basilar arteryen_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.doi10.1038/jcbfm.1993.64-
dc.identifier.pmid8478408-
dc.identifier.scopuseid_2-s2.0-0027253401en_US
dc.identifier.volume13en_US
dc.identifier.issue3en_US
dc.identifier.spage498en_US
dc.identifier.epage502en_US
dc.identifier.isiWOS:A1993KY45800017-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridNagao, T=7401489430en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.issnl0271-678X-

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