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Article: Inhibition of ultra-rapid delayed rectifier K + current by verapamil in human atrial myocytes

TitleInhibition of ultra-rapid delayed rectifier K + current by verapamil in human atrial myocytes
Authors
Issue Date2004
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yjmcc
Citation
Journal Of Molecular And Cellular Cardiology, 2004, v. 36 n. 2, p. 257-263 How to Cite?
AbstractVerapamil is a widely used Ca 2+ channel antagonist in the treatment of cardiovascular disorders including atrial arrhythmias. However, it is unknown whether the drug would inhibit the repolarization currents transient outward K + current (I to1) and ultra-rapid delayed rectifier K + current (I Kur) in human atrium. With whole-cell patch configuration, we evaluated effects of verapamil on I to1 and I Kur in isolated human atrial myocytes. It was found that verapamil did not decrease I to1 at 1-50 μM. However, verapamil reversibly inhibited I Kur in a concentration-dependent manner (IC 50 = 3.2 μM). At test potential of +50 mV, 5 μM verapamil decreased I Kur by 61.3 ± 7.5%. Verapamil significantly accelerated inactivation of I Kur, suggesting an open channel block mechanism. The results indicate that verapamil significantly blocks the repolarization K + current I Kur, but not I to1, in human atrial atrium, which may account at least in part for the atrial effect of the drug. © 2003 Elsevier Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/162763
ISSN
2015 Impact Factor: 4.874
2015 SCImago Journal Rankings: 2.522
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorGao, Zen_US
dc.contributor.authorLau, CPen_US
dc.contributor.authorChiu, SWen_US
dc.contributor.authorLi, GRen_US
dc.date.accessioned2012-09-05T05:23:10Z-
dc.date.available2012-09-05T05:23:10Z-
dc.date.issued2004en_US
dc.identifier.citationJournal Of Molecular And Cellular Cardiology, 2004, v. 36 n. 2, p. 257-263en_US
dc.identifier.issn0022-2828en_US
dc.identifier.urihttp://hdl.handle.net/10722/162763-
dc.description.abstractVerapamil is a widely used Ca 2+ channel antagonist in the treatment of cardiovascular disorders including atrial arrhythmias. However, it is unknown whether the drug would inhibit the repolarization currents transient outward K + current (I to1) and ultra-rapid delayed rectifier K + current (I Kur) in human atrium. With whole-cell patch configuration, we evaluated effects of verapamil on I to1 and I Kur in isolated human atrial myocytes. It was found that verapamil did not decrease I to1 at 1-50 μM. However, verapamil reversibly inhibited I Kur in a concentration-dependent manner (IC 50 = 3.2 μM). At test potential of +50 mV, 5 μM verapamil decreased I Kur by 61.3 ± 7.5%. Verapamil significantly accelerated inactivation of I Kur, suggesting an open channel block mechanism. The results indicate that verapamil significantly blocks the repolarization K + current I Kur, but not I to1, in human atrial atrium, which may account at least in part for the atrial effect of the drug. © 2003 Elsevier Ltd. All rights reserved.en_US
dc.languageengen_US
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yjmccen_US
dc.relation.ispartofJournal of Molecular and Cellular Cardiologyen_US
dc.subject.mesh4-Aminopyridine - Pharmacologyen_US
dc.subject.meshAdulten_US
dc.subject.meshAgeden_US
dc.subject.meshCalcium-Binding Protein, Vitamin D-Dependenten_US
dc.subject.meshCoronary Disease - Physiopathology - Surgeryen_US
dc.subject.meshHeart Atria - Physiopathologyen_US
dc.subject.meshHumansen_US
dc.subject.meshKineticsen_US
dc.subject.meshMembrane Potentials - Drug Effects - Physiologyen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshMuscle Cells - Drug Effects - Physiologyen_US
dc.subject.meshPotassium Channels, Inwardly Rectifying - Antagonists & Inhibitors - Physiologyen_US
dc.subject.meshVerapamil - Pharmacologyen_US
dc.titleInhibition of ultra-rapid delayed rectifier K + current by verapamil in human atrial myocytesen_US
dc.typeArticleen_US
dc.identifier.emailLi, GR:grli@hkucc.hku.hken_US
dc.identifier.authorityLi, GR=rp00476en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.yjmcc.2003.11.003en_US
dc.identifier.pmid14871553-
dc.identifier.scopuseid_2-s2.0-1042286368en_US
dc.identifier.hkuros88553-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-1042286368&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume36en_US
dc.identifier.issue2en_US
dc.identifier.spage257en_US
dc.identifier.epage263en_US
dc.identifier.isiWOS:000189264800011-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridGao, Z=16549711200en_US
dc.identifier.scopusauthoridLau, CP=7401968501en_US
dc.identifier.scopusauthoridChiu, SW=12788356600en_US
dc.identifier.scopusauthoridLi, GR=7408462932en_US

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