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Article: Effects of chromanol 293B on transient outward and ultra-rapid delayed rectifier potassium currents in human atrial myocytes

TitleEffects of chromanol 293B on transient outward and ultra-rapid delayed rectifier potassium currents in human atrial myocytes
Authors
Issue Date2003
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yjmcc
Citation
Journal Of Molecular And Cellular Cardiology, 2003, v. 35 n. 3, p. 293-300 How to Cite?
AbstractIt is unclear whether chromanol 293B, a selective inhibitor of slow component of delayed rectifier K+ current (IKs), may affect other K+ currents in human atrium. With whole-cell patch configuration, we evaluated effects of 293B on transient outward K+ current (Ito1) and ultra-rapid delayed rectifier K+ current (IKur) in isolated human atrial myocytes. It was found that 293B inhibited Ito1 and IKur in a concentration-dependent manner. At 10 μM 293B suppressed Ito1 to 3.4 ± 0.4 from 5.1 ± 0.3 pA/pF (P < 0.01), and IKur to 1.5 ± 0.2 from 2.1 ± 0.3 pA/pF (P < 0.01) at +50 mV. The inhibition of Ito1 and IKur was independent of depolarizing voltage, and the concentration of 50% inhibition was 31.2 μM for Ito1, and 30.9 μM for IKur. 293B blocked Ito1 and IKur with the same concentration range, and the significant effect was observed from the concentration of 1 μM. The maximum inhibitive effect was 88% for Ito1 and 96% for IKur at 250 μM. Voltage dependence of activation and inactivation, and time-dependent recovery from inactivation of Ito1 were not altered by 293B; however, time to peak and time-dependent inactivation of Ito1 was significantly accelerated. The results indicate that 293B significantly inhibits the major repolarization K+ currents Ito1 and IKur in human atrial myocytes. © 2003 Elsevier Science Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/162674
ISSN
2015 Impact Factor: 4.874
2015 SCImago Journal Rankings: 2.522
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorDu, XLen_US
dc.contributor.authorLau, CPen_US
dc.contributor.authorChiu, SWen_US
dc.contributor.authorTse, HFen_US
dc.contributor.authorGerlach, Uen_US
dc.contributor.authorLi, GRen_US
dc.date.accessioned2012-09-05T05:22:14Z-
dc.date.available2012-09-05T05:22:14Z-
dc.date.issued2003en_US
dc.identifier.citationJournal Of Molecular And Cellular Cardiology, 2003, v. 35 n. 3, p. 293-300en_US
dc.identifier.issn0022-2828en_US
dc.identifier.urihttp://hdl.handle.net/10722/162674-
dc.description.abstractIt is unclear whether chromanol 293B, a selective inhibitor of slow component of delayed rectifier K+ current (IKs), may affect other K+ currents in human atrium. With whole-cell patch configuration, we evaluated effects of 293B on transient outward K+ current (Ito1) and ultra-rapid delayed rectifier K+ current (IKur) in isolated human atrial myocytes. It was found that 293B inhibited Ito1 and IKur in a concentration-dependent manner. At 10 μM 293B suppressed Ito1 to 3.4 ± 0.4 from 5.1 ± 0.3 pA/pF (P < 0.01), and IKur to 1.5 ± 0.2 from 2.1 ± 0.3 pA/pF (P < 0.01) at +50 mV. The inhibition of Ito1 and IKur was independent of depolarizing voltage, and the concentration of 50% inhibition was 31.2 μM for Ito1, and 30.9 μM for IKur. 293B blocked Ito1 and IKur with the same concentration range, and the significant effect was observed from the concentration of 1 μM. The maximum inhibitive effect was 88% for Ito1 and 96% for IKur at 250 μM. Voltage dependence of activation and inactivation, and time-dependent recovery from inactivation of Ito1 were not altered by 293B; however, time to peak and time-dependent inactivation of Ito1 was significantly accelerated. The results indicate that 293B significantly inhibits the major repolarization K+ currents Ito1 and IKur in human atrial myocytes. © 2003 Elsevier Science 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.meshAdulten_US
dc.subject.meshAgeden_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshChromans - Pharmacologyen_US
dc.subject.meshDelayed Rectifier Potassium Channelsen_US
dc.subject.meshHeart Atria - Cytologyen_US
dc.subject.meshHumansen_US
dc.subject.meshMembrane Potentialsen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshMyocytes, Cardiac - Drug Effects - Physiologyen_US
dc.subject.meshPatch-Clamp Techniquesen_US
dc.subject.meshPotassium Channel Blockers - Pharmacologyen_US
dc.subject.meshPotassium Channels - Physiologyen_US
dc.subject.meshPotassium Channels, Tandem Pore Domainen_US
dc.subject.meshPotassium Channels, Voltage-Gateden_US
dc.subject.meshSulfonamides - Pharmacologyen_US
dc.titleEffects of chromanol 293B on transient outward and ultra-rapid delayed rectifier potassium currents in human atrial myocytesen_US
dc.typeArticleen_US
dc.identifier.emailTse, HF:hftse@hkucc.hku.hken_US
dc.identifier.emailLi, GR:grli@hkucc.hku.hken_US
dc.identifier.authorityTse, HF=rp00428en_US
dc.identifier.authorityLi, GR=rp00476en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/S0022-2828(03)00007-5en_US
dc.identifier.pmid12676544-
dc.identifier.scopuseid_2-s2.0-0037350080en_US
dc.identifier.hkuros100806-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037350080&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume35en_US
dc.identifier.issue3en_US
dc.identifier.spage293en_US
dc.identifier.epage300en_US
dc.identifier.isiWOS:000182212600008-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridDu, XL=9036718000en_US
dc.identifier.scopusauthoridLau, CP=7401968501en_US
dc.identifier.scopusauthoridChiu, SW=12788356600en_US
dc.identifier.scopusauthoridTse, HF=7006070805en_US
dc.identifier.scopusauthoridGerlach, U=7005770400en_US
dc.identifier.scopusauthoridLi, GR=7408462932en_US

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