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Article: Human Kir2.1 channel carries a transient outward potassium current with inward rectification

TitleHuman Kir2.1 channel carries a transient outward potassium current with inward rectification
Authors
Issue Date2009
PublisherSpringer. The Journal's web site is located at http://link.springer.de/link/service/journals/00424/index.htm
Citation
Pflugers Archiv European Journal Of Physiology, 2009, v. 457 n. 6, p. 1275-1285 How to Cite?
AbstractWe have previously reported a depolarization-activated 4-aminopyridine- resistant transient outward K+ current with inward rectification (I to.ir) in canine and guinea pig cardiac myocytes. However, molecular identity of this current is not clear. The present study was designed to investigate whether Kir2.1 channel carries this current in stably transfected human embryonic kidney (HEK) 293 cells using whole-cell patch-clamp technique. It was found that HEK 293 cells stably expressing human Kir2.1 gene had a transient outward current elicited by voltage steps positive to the membrane potential (around -70 mV). The current exhibited a current-voltage relationship with intermediate inward rectification and showed time-dependent inactivation and rapid recovery from inactivation. The half potential (V 0.5) of availability of the current was -49.4∈±∈2.1 mV at 5 mM K + in bath solution. Action potential waveform clamp revealed two components of outward currents; one was immediately elicited and then rapidly inactivated during depolarization, and another was slowly activated during repolarization of action potential. These properties were similar to those of I to.ir observed previously in native cardiac myocytes. Interestingly, inactivation of the I to.ir was strongly slowed by increasing intracellular free Mg2+ (Mg2+ i , from 0.03 to 1.0, 4.0, and 8.0 mM). The component elicited by action potential depolarization increased with the elevation of Mg2+ i . Inclusion of spermine (100 μM) in the pipette solution remarkably inhibited both the I to.ir and steady-state current. These results demonstrate that the Mg2+ i -dependent current carried by Kir2.1 likely is the molecular identity of I to.ir observed previously in cardiac myocytes. © 2008 Springer-Verlag.
Persistent Identifierhttp://hdl.handle.net/10722/163237
ISSN
2015 Impact Factor: 3.654
2015 SCImago Journal Rankings: 1.638
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhang, DYen_US
dc.contributor.authorLau, CPen_US
dc.contributor.authorLi, GRen_US
dc.date.accessioned2012-09-05T05:29:02Z-
dc.date.available2012-09-05T05:29:02Z-
dc.date.issued2009en_US
dc.identifier.citationPflugers Archiv European Journal Of Physiology, 2009, v. 457 n. 6, p. 1275-1285en_US
dc.identifier.issn0031-6768en_US
dc.identifier.urihttp://hdl.handle.net/10722/163237-
dc.description.abstractWe have previously reported a depolarization-activated 4-aminopyridine- resistant transient outward K+ current with inward rectification (I to.ir) in canine and guinea pig cardiac myocytes. However, molecular identity of this current is not clear. The present study was designed to investigate whether Kir2.1 channel carries this current in stably transfected human embryonic kidney (HEK) 293 cells using whole-cell patch-clamp technique. It was found that HEK 293 cells stably expressing human Kir2.1 gene had a transient outward current elicited by voltage steps positive to the membrane potential (around -70 mV). The current exhibited a current-voltage relationship with intermediate inward rectification and showed time-dependent inactivation and rapid recovery from inactivation. The half potential (V 0.5) of availability of the current was -49.4∈±∈2.1 mV at 5 mM K + in bath solution. Action potential waveform clamp revealed two components of outward currents; one was immediately elicited and then rapidly inactivated during depolarization, and another was slowly activated during repolarization of action potential. These properties were similar to those of I to.ir observed previously in native cardiac myocytes. Interestingly, inactivation of the I to.ir was strongly slowed by increasing intracellular free Mg2+ (Mg2+ i , from 0.03 to 1.0, 4.0, and 8.0 mM). The component elicited by action potential depolarization increased with the elevation of Mg2+ i . Inclusion of spermine (100 μM) in the pipette solution remarkably inhibited both the I to.ir and steady-state current. These results demonstrate that the Mg2+ i -dependent current carried by Kir2.1 likely is the molecular identity of I to.ir observed previously in cardiac myocytes. © 2008 Springer-Verlag.en_US
dc.languageengen_US
dc.publisherSpringer. The Journal's web site is located at http://link.springer.de/link/service/journals/00424/index.htmen_US
dc.relation.ispartofPflugers Archiv European Journal of Physiologyen_US
dc.subject.meshAction Potentials - Physiologyen_US
dc.subject.meshCell Lineen_US
dc.subject.meshHumansen_US
dc.subject.meshKidney - Embryologyen_US
dc.subject.meshMagnesium - Metabolismen_US
dc.subject.meshMembrane Potentials - Physiologyen_US
dc.subject.meshMyocytes, Cardiac - Physiologyen_US
dc.subject.meshPatch-Clamp Techniquesen_US
dc.subject.meshPotassium Channels, Inwardly Rectifying - Drug Effects - Physiologyen_US
dc.subject.meshSpermine - Pharmacologyen_US
dc.titleHuman Kir2.1 channel carries a transient outward potassium current with inward rectificationen_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.doi10.1007/s00424-008-0608-0en_US
dc.identifier.pmid19002489-
dc.identifier.scopuseid_2-s2.0-62549112999en_US
dc.identifier.hkuros156315-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-62549112999&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume457en_US
dc.identifier.issue6en_US
dc.identifier.spage1275en_US
dc.identifier.epage1285en_US
dc.identifier.isiWOS:000264184300007-
dc.publisher.placeGermanyen_US
dc.identifier.scopusauthoridZhang, DY=24588358100en_US
dc.identifier.scopusauthoridLau, CP=7401968501en_US
dc.identifier.scopusauthoridLi, GR=7408462932en_US
dc.identifier.citeulike3627764-

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