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Article: Transmembrane I(Ca) contributes to rate-dependent changes of action potentials in human ventricular myocytes

TitleTransmembrane I(Ca) contributes to rate-dependent changes of action potentials in human ventricular myocytes
Authors
Issue Date1999
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/
Citation
American Journal Of Physiology - Heart And Circulatory Physiology, 1999, v. 276 n. 1 45-1, p. H98-H106 How to Cite?
AbstractThe mechanism of action potential abbreviation caused by increasing rate in human ventricular myocytes is unknown. The present study was designed to determine the potential role of Ca2+ current (I(Ca)) in the rate-dependent changes in action potential duration (APD) in human ventricular cells. Myocytes isolated from the right ventricle of explanted human hearts were studied at 36°C with whole cell voltage and current-clamp techniques. APD at 90% repolarization decreased by 36 ± 4% when frequency increased from 0.5 to 2 Hz. Equimolar substitution of Mg2+ for Ca2+ significantly decreased rate-dependent changes in APD (to 6 ± 3%, P < 0.01). Peak I(Ca) was decreased by 34 ± 3% from 0.5 to 2 Hz (P < 0.01), and I(Ca) had recovery time constants of 65 ± 12 and 683 ± 39 ms at -80 mV. Action potential clamp demonstrated a decreasing contribution of I(Ca) during the action potential as rate increased. The rate-dependent slow component of the delayed rectifier K+ current (I(Ks)) was not observed in four cells with an increase in frequency from 0.5 to 3.3 Hz, perhaps because the I(Ks) is so small that the increase at a high rate could not be seen. These results suggest that reduction of Ca2+ influx during the action potential accounts for most of the rate-dependent abbreviation of human ventricular APD.
Persistent Identifierhttp://hdl.handle.net/10722/162271
ISSN
2015 Impact Factor: 3.324
2015 SCImago Journal Rankings: 1.823
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLi, GRen_US
dc.contributor.authorYang, Ben_US
dc.contributor.authorFeng, Jen_US
dc.contributor.authorBosch, RFen_US
dc.contributor.authorCarrier, Men_US
dc.contributor.authorNattel, Sen_US
dc.date.accessioned2012-09-05T05:18:33Z-
dc.date.available2012-09-05T05:18:33Z-
dc.date.issued1999en_US
dc.identifier.citationAmerican Journal Of Physiology - Heart And Circulatory Physiology, 1999, v. 276 n. 1 45-1, p. H98-H106en_US
dc.identifier.issn0363-6135en_US
dc.identifier.urihttp://hdl.handle.net/10722/162271-
dc.description.abstractThe mechanism of action potential abbreviation caused by increasing rate in human ventricular myocytes is unknown. The present study was designed to determine the potential role of Ca2+ current (I(Ca)) in the rate-dependent changes in action potential duration (APD) in human ventricular cells. Myocytes isolated from the right ventricle of explanted human hearts were studied at 36°C with whole cell voltage and current-clamp techniques. APD at 90% repolarization decreased by 36 ± 4% when frequency increased from 0.5 to 2 Hz. Equimolar substitution of Mg2+ for Ca2+ significantly decreased rate-dependent changes in APD (to 6 ± 3%, P < 0.01). Peak I(Ca) was decreased by 34 ± 3% from 0.5 to 2 Hz (P < 0.01), and I(Ca) had recovery time constants of 65 ± 12 and 683 ± 39 ms at -80 mV. Action potential clamp demonstrated a decreasing contribution of I(Ca) during the action potential as rate increased. The rate-dependent slow component of the delayed rectifier K+ current (I(Ks)) was not observed in four cells with an increase in frequency from 0.5 to 3.3 Hz, perhaps because the I(Ks) is so small that the increase at a high rate could not be seen. These results suggest that reduction of Ca2+ influx during the action potential accounts for most of the rate-dependent abbreviation of human ventricular APD.en_US
dc.languageengen_US
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/en_US
dc.relation.ispartofAmerican Journal of Physiology - Heart and Circulatory Physiologyen_US
dc.subject.meshAction Potentials - Physiologyen_US
dc.subject.meshCalcium - Physiologyen_US
dc.subject.meshCell Membrane - Physiologyen_US
dc.subject.meshElectric Conductivityen_US
dc.subject.meshHumansen_US
dc.subject.meshMyocardium - Cytologyen_US
dc.subject.meshPatch-Clamp Techniquesen_US
dc.subject.meshPotassium - Physiologyen_US
dc.subject.meshReaction Time - Physiologyen_US
dc.subject.meshVentricular Function - Physiologyen_US
dc.titleTransmembrane I(Ca) contributes to rate-dependent changes of action potentials in human ventricular 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.pmid9887022-
dc.identifier.scopuseid_2-s2.0-0032615454en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032615454&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume276en_US
dc.identifier.issue1 45-1en_US
dc.identifier.spageH98en_US
dc.identifier.epageH106en_US
dc.identifier.isiWOS:000078108600014-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLi, GR=7408462932en_US
dc.identifier.scopusauthoridYang, B=7404472748en_US
dc.identifier.scopusauthoridFeng, J=7403884361en_US
dc.identifier.scopusauthoridBosch, RF=7102263519en_US
dc.identifier.scopusauthoridCarrier, M=7101604979en_US
dc.identifier.scopusauthoridNattel, S=36048738800en_US

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