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Conference Paper: Distinctive density, biophysical properties, and pharmacology of voltage-gated sodium current in atrial and ventricular myocytes

TitleDistinctive density, biophysical properties, and pharmacology of voltage-gated sodium current in atrial and ventricular myocytes
Authors
KeywordsMedical sciences
Cardiovascular diseases
Issue Date2013
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/heartrhythmjournal
Citation
The 34th Annual Scientific Sessions of the Heart Rhythm Society (Heart Rhythm 2013). Denver, CO., 8-11 May 2013. In Heart Rhythm, 2013, v. 10 n. 5 suppl., p. S322 How to Cite?
AbstractBACKGROUND AND OBJECTIVE: Our earlier study reported that heterogeneous voltage-gated sodium current (INa) in the density and biophysical properties is present in atrial and ventricular myocytes from guinea pig heart (Li et al, J Mol Cell Cardiol 2002;34:1185-1194). However, molecular contribution is not understood for the different properties of INa in atrial and ventricular myocytes of the heart. The present study was designed to investigate the properties, potential molecular contribution, and pharmacology of INa in atrial and ventricular myocytes of rat heart using approaches of electrophysiology and molecular biology. RESULTS: It was found the INa density (-35 mV) was greater in left atrial (n=17, -38.6±4.6 pA/pF) than that in left ventricular (n=35, -24.5±1.3 pA/pF, P<0.01) myocytes. Time constants of activation (τm) and inactivation (τh) of INa was smaller in atrial (0.23±0.02 ms and 1.05±0.04 ms) than those in ventricular (0.48±0.02 ms and 1.67±0.06 ms, P<0.01) myocytes. The V1/2 of INa availability (I/Imax) was more negative in atrial (n=15, -100.3±1.1 mV) than that in ventricular (n=18, -95.1±1.0 mV, P<0.05) myocytes. In addition, recovery of INa from inactivation was slower in atrial than that in ventricular myocytes. Molecular biological experiments revealed that mRNAs and proteins of SCN5A, SCN4A, SCN10A, SCN1B, SCN2B, and SCN3B were homogenously expressed in both atrial and ventricular myocytes. Interestingly, expression of SCN4B was greater (2.8 folds) in ventricular myocytes than that in atrial myocytes. The anti-arrhythmic drug quinidine inhibited INa with IC50 of 2.8 μM in atrial myocytes, while 7.2 μM in ventricular myocytes. CONCLUSIONS: Our results demonstrate for the first time to our knowledge that distinctive density and biophysical properties of INa are present in atrial and ventricular myocytes of from rat heart. The less expression of SCN4B in atrial myocytes likely contributes at least in part to the higher density, quicker activation and inactivation, negative potential of inactivation, slower recovery from inactivation of INa, and the more sensitive to inhibition by the anti-arrhythmic drug quinidine. The study further supports the notion that atrial INa may be a target for developing atrial selective anti-atrial fibrillation drug.
DescriptionThis journal suppl. entitled: Heart Rhythm 2013 34th Annual Scientific Sessions
Poster Session IV
Persistent Identifierhttp://hdl.handle.net/10722/183906
ISSN
2015 Impact Factor: 4.391
2015 SCImago Journal Rankings: 2.756

 

DC FieldValueLanguage
dc.contributor.authorLi, GRen_US
dc.contributor.authorChen, Ken_US
dc.contributor.authorSun, Hen_US
dc.date.accessioned2013-06-18T04:26:01Z-
dc.date.available2013-06-18T04:26:01Z-
dc.date.issued2013en_US
dc.identifier.citationThe 34th Annual Scientific Sessions of the Heart Rhythm Society (Heart Rhythm 2013). Denver, CO., 8-11 May 2013. In Heart Rhythm, 2013, v. 10 n. 5 suppl., p. S322en_US
dc.identifier.issn1547-5271-
dc.identifier.urihttp://hdl.handle.net/10722/183906-
dc.descriptionThis journal suppl. entitled: Heart Rhythm 2013 34th Annual Scientific Sessions-
dc.descriptionPoster Session IV-
dc.description.abstractBACKGROUND AND OBJECTIVE: Our earlier study reported that heterogeneous voltage-gated sodium current (INa) in the density and biophysical properties is present in atrial and ventricular myocytes from guinea pig heart (Li et al, J Mol Cell Cardiol 2002;34:1185-1194). However, molecular contribution is not understood for the different properties of INa in atrial and ventricular myocytes of the heart. The present study was designed to investigate the properties, potential molecular contribution, and pharmacology of INa in atrial and ventricular myocytes of rat heart using approaches of electrophysiology and molecular biology. RESULTS: It was found the INa density (-35 mV) was greater in left atrial (n=17, -38.6±4.6 pA/pF) than that in left ventricular (n=35, -24.5±1.3 pA/pF, P<0.01) myocytes. Time constants of activation (τm) and inactivation (τh) of INa was smaller in atrial (0.23±0.02 ms and 1.05±0.04 ms) than those in ventricular (0.48±0.02 ms and 1.67±0.06 ms, P<0.01) myocytes. The V1/2 of INa availability (I/Imax) was more negative in atrial (n=15, -100.3±1.1 mV) than that in ventricular (n=18, -95.1±1.0 mV, P<0.05) myocytes. In addition, recovery of INa from inactivation was slower in atrial than that in ventricular myocytes. Molecular biological experiments revealed that mRNAs and proteins of SCN5A, SCN4A, SCN10A, SCN1B, SCN2B, and SCN3B were homogenously expressed in both atrial and ventricular myocytes. Interestingly, expression of SCN4B was greater (2.8 folds) in ventricular myocytes than that in atrial myocytes. The anti-arrhythmic drug quinidine inhibited INa with IC50 of 2.8 μM in atrial myocytes, while 7.2 μM in ventricular myocytes. CONCLUSIONS: Our results demonstrate for the first time to our knowledge that distinctive density and biophysical properties of INa are present in atrial and ventricular myocytes of from rat heart. The less expression of SCN4B in atrial myocytes likely contributes at least in part to the higher density, quicker activation and inactivation, negative potential of inactivation, slower recovery from inactivation of INa, and the more sensitive to inhibition by the anti-arrhythmic drug quinidine. The study further supports the notion that atrial INa may be a target for developing atrial selective anti-atrial fibrillation drug.-
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/heartrhythmjournal-
dc.relation.ispartofHeart Rhythmen_US
dc.subjectMedical sciences-
dc.subjectCardiovascular diseases-
dc.titleDistinctive density, biophysical properties, and pharmacology of voltage-gated sodium current in atrial and ventricular myocytesen_US
dc.typeConference_Paperen_US
dc.identifier.emailLi, GR: grli@hkucc.hku.hken_US
dc.identifier.emailChen, K: chenkh@hku.hken_US
dc.identifier.emailSun, H: hysun@hkucc.hku.hken_US
dc.identifier.authorityLi, GR=rp00476en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1016/j.hrthm.2013.03.031-
dc.identifier.hkuros214567en_US
dc.identifier.volume10en_US
dc.identifier.issue5 suppl.en_US
dc.identifier.spageS322en_US
dc.identifier.epageS322en_US
dc.publisher.placeUnited States-

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