File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Isoproterenol causes hyperpolarization through opening of ATP-sensitive potassium channels in vascular smooth muscle of the canine saphenous vein

TitleIsoproterenol causes hyperpolarization through opening of ATP-sensitive potassium channels in vascular smooth muscle of the canine saphenous vein
Authors
Issue Date1995
PublisherAmerican Society for Pharmacology and Experimental Therapeutics. The Journal's web site is located at http://jpet.aspetjournals.org
Citation
Journal Of Pharmacology And Experimental Therapeutics, 1995, v. 272 n. 1, p. 379-384 How to Cite?
AbstractExperiments were designed to determine how isoproterenol affects the cell membrane potential of smooth muscle cells of the canine saphenous vein. Measurements of membrane potential were performed using glass microelectrodes. Isoproterenol (10-9 to 10-6 M) caused sustained, concentration-dependent membrane hyperpolarizations in tissues with and without endothelium. ICI 118,551 (a selective β2-adrenoceptor antagonist), but not atenolol (a selective β1-adrenoceptor antagonist), abolished the hyperpolarization to isoproterenol. Forskolin, an activator of adenylate cyclase, produced sustained hyperpolarizations, which were not mimicked by 1,9-dideoxyforskolin. Incubation with either ouabain or extracellular K+- free solution did not inhibit the electrical response to isoproterenol. Glibenclamide (a selective ATP-sensitive K+ channel antagonist) attenuated the hyperpolarizations induced by either isoproterenol or forskolin, whereas charybdotoxin (an inhibitor of large conductance Ca++-activated K+ channels) did not. These findings suggest that isoproterenol opens ATP- sensitive K+ channels indirectly through activation of adenylate cyclase in the smooth muscle of the canine saphenous vein. The adrenergic receptor involved belongs to the β2-adrenoceptor subtype.
Persistent Identifierhttp://hdl.handle.net/10722/171156
ISSN
2015 Impact Factor: 3.76
2015 SCImago Journal Rankings: 1.847

 

DC FieldValueLanguage
dc.contributor.authorNakashima, Men_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:26Z-
dc.date.available2012-10-30T06:12:26Z-
dc.date.issued1995en_US
dc.identifier.citationJournal Of Pharmacology And Experimental Therapeutics, 1995, v. 272 n. 1, p. 379-384en_US
dc.identifier.issn0022-3565en_US
dc.identifier.urihttp://hdl.handle.net/10722/171156-
dc.description.abstractExperiments were designed to determine how isoproterenol affects the cell membrane potential of smooth muscle cells of the canine saphenous vein. Measurements of membrane potential were performed using glass microelectrodes. Isoproterenol (10-9 to 10-6 M) caused sustained, concentration-dependent membrane hyperpolarizations in tissues with and without endothelium. ICI 118,551 (a selective β2-adrenoceptor antagonist), but not atenolol (a selective β1-adrenoceptor antagonist), abolished the hyperpolarization to isoproterenol. Forskolin, an activator of adenylate cyclase, produced sustained hyperpolarizations, which were not mimicked by 1,9-dideoxyforskolin. Incubation with either ouabain or extracellular K+- free solution did not inhibit the electrical response to isoproterenol. Glibenclamide (a selective ATP-sensitive K+ channel antagonist) attenuated the hyperpolarizations induced by either isoproterenol or forskolin, whereas charybdotoxin (an inhibitor of large conductance Ca++-activated K+ channels) did not. These findings suggest that isoproterenol opens ATP- sensitive K+ channels indirectly through activation of adenylate cyclase in the smooth muscle of the canine saphenous vein. The adrenergic receptor involved belongs to the β2-adrenoceptor subtype.en_US
dc.languageengen_US
dc.publisherAmerican Society for Pharmacology and Experimental Therapeutics. The Journal's web site is located at http://jpet.aspetjournals.orgen_US
dc.relation.ispartofJournal of Pharmacology and Experimental Therapeuticsen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAtenolol - Pharmacologyen_US
dc.subject.meshCharybdotoxinen_US
dc.subject.meshDogsen_US
dc.subject.meshFemaleen_US
dc.subject.meshForskolin - Pharmacologyen_US
dc.subject.meshGlyburide - Pharmacologyen_US
dc.subject.meshIon Channel Gating - Drug Effectsen_US
dc.subject.meshIsoproterenol - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMembrane Potentials - Drug Effectsen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effectsen_US
dc.subject.meshOuabain - Pharmacologyen_US
dc.subject.meshPotassium Channels - Drug Effectsen_US
dc.subject.meshPropanolamines - Pharmacologyen_US
dc.subject.meshReceptors, Adrenergic, Beta - Drug Effectsen_US
dc.subject.meshSaphenous Veinen_US
dc.subject.meshScorpion Venoms - Pharmacologyen_US
dc.subject.meshYohimbine - Pharmacologyen_US
dc.titleIsoproterenol causes hyperpolarization through opening of ATP-sensitive potassium channels in vascular smooth muscle of the canine saphenous veinen_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.pmid7529310-
dc.identifier.scopuseid_2-s2.0-0028893949en_US
dc.identifier.volume272en_US
dc.identifier.issue1en_US
dc.identifier.spage379en_US
dc.identifier.epage384en_US
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridNakashima, M=35599797500en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats