File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Effects of diltiazem and nifedipine on transient outward and ultra-rapid delayed rectifier potassium currents in human atrial myocytes

TitleEffects of diltiazem and nifedipine on transient outward and ultra-rapid delayed rectifier potassium currents in human atrial myocytes
Authors
Gao, ZSun, HChiu, SWLau, CPLi, GR
KeywordsDiltiazem
Human atrial myocyte
Ion channels
Nifedipine
Transient outward K + current
Ultra-rapid delayed rectifier K + current
Issue Date2005
PublisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1
Citation
British Journal of Pharmacology, 2005, v. 144 n. 4, p. 595-604 How to Cite?
DOI: http://dx.doi.org/10.1038/sj.bjp.0706113
AbstractIt is unknown whether the widely used L-type Ca 2+ channel antagonists diltiazem and nifedipine would block the repolarization K + currents, transient outward current (I tol) and ultra-rapid delayed rectifier K + current (I Kur), in human atrium. The present study was to determine the effects of diltiazem and nifedipine on I tol and I Kur in human atrial myocytes with whole-cell patch-clamp technique. It was found that diltiazem substantially inhibited I tol in a concentration-dependent manner, with an IC 50 of 29.2 ± 2.4 μM, and nifedipine showed a similar effect (IC 50 = 26.8 ± 2.1 μM). The two drugs had no effect on voltage-dependent kinetics of the current; however, they accelerated I tol inactivation significantly, suggesting an open channel block. In addition, diltiazem and nifedipine suppressed I Kur in a concentration-dependent manner (at + 50 mV, IC 50 = 11.2 ± 0.9 and 8.2 ± 0.8 μM, respectively). These results indicate that the Ca 2+ channel blockers diltiazem and nifedipine substantially inhibit I tol and I Kur in human atrial myocytes. © 2005 Nature Publishing Group All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/49036
ISSN
0007-1188
2023 Impact Factor: 6.8
2023 SCImago Journal Rankings: 2.119
PubMed Central ID
PMC1576039
ISI Accession Number ID
WOS:000227330600017
References
References in Scopus

 

DC FieldValueLanguage
dc.contributor.authorGao, Zen_HK
dc.contributor.authorSun, Hen_HK
dc.contributor.authorChiu, SWen_HK
dc.contributor.authorLau, CPen_HK
dc.contributor.authorLi, GRen_HK
dc.date.accessioned2008-06-12T06:33:01Z-
dc.date.available2008-06-12T06:33:01Z-
dc.date.issued2005en_HK
dc.identifier.citationBritish Journal of Pharmacology, 2005, v. 144 n. 4, p. 595-604en_HK
dc.identifier.issn0007-1188en_HK
dc.identifier.urihttp://hdl.handle.net/10722/49036-
dc.description.abstractIt is unknown whether the widely used L-type Ca 2+ channel antagonists diltiazem and nifedipine would block the repolarization K + currents, transient outward current (I tol) and ultra-rapid delayed rectifier K + current (I Kur), in human atrium. The present study was to determine the effects of diltiazem and nifedipine on I tol and I Kur in human atrial myocytes with whole-cell patch-clamp technique. It was found that diltiazem substantially inhibited I tol in a concentration-dependent manner, with an IC 50 of 29.2 ± 2.4 μM, and nifedipine showed a similar effect (IC 50 = 26.8 ± 2.1 μM). The two drugs had no effect on voltage-dependent kinetics of the current; however, they accelerated I tol inactivation significantly, suggesting an open channel block. In addition, diltiazem and nifedipine suppressed I Kur in a concentration-dependent manner (at + 50 mV, IC 50 = 11.2 ± 0.9 and 8.2 ± 0.8 μM, respectively). These results indicate that the Ca 2+ channel blockers diltiazem and nifedipine substantially inhibit I tol and I Kur in human atrial myocytes. © 2005 Nature Publishing Group All rights reserved.en_HK
dc.format.extent388 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1en_HK
dc.relation.ispartofBritish Journal of Pharmacologyen_HK
dc.subjectDiltiazemen_HK
dc.subjectHuman atrial myocyteen_HK
dc.subjectIon channelsen_HK
dc.subjectNifedipineen_HK
dc.subjectTransient outward K + currenten_HK
dc.subjectUltra-rapid delayed rectifier K + currenten_HK
dc.titleEffects of diltiazem and nifedipine on transient outward and ultra-rapid delayed rectifier potassium currents in human atrial myocytesen_HK
dc.typeArticleen_HK
dc.identifier.emailLi, GR:grli@hkucc.hku.hken_HK
dc.identifier.authorityLi, GR=rp00476en_HK
dc.description.naturelink_to_OA_fulltexten_HK
dc.identifier.doi10.1038/sj.bjp.0706113en_HK
dc.identifier.pmid15678082-
dc.identifier.pmcidPMC1576039en_HK
dc.identifier.scopuseid_2-s2.0-14844323679en_HK
dc.identifier.hkuros101183-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-14844323679&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume144en_HK
dc.identifier.issue4en_HK
dc.identifier.spage595en_HK
dc.identifier.epage604en_HK
dc.identifier.isiWOS:000227330600017-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridGao, Z=16549711200en_HK
dc.identifier.scopusauthoridSun, H=35723049200en_HK
dc.identifier.scopusauthoridChiu, SW=12788356600en_HK
dc.identifier.scopusauthoridLau, CP=7401968501en_HK
dc.identifier.scopusauthoridLi, GR=7408462932en_HK
dc.identifier.issnl0007-1188-

Export via OAI-PMH Interface in XML Formats

OR

Export to Other Non-XML Formats