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Cardiovascular Research 2007 74(3):356-365; doi:10.1016/j.cardiores.2007.01.009
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Copyright © 2007, European Society of Cardiology

SCN5A and sinoatrial node pacemaker function

Ming Leia,*, Henggui Zhangb, Andrew A. Gracec and Christopher L.-H. Huangc

aCardiovascular Group, School of Medicine, The University of Manchester, Manchester, M13, 9NT, UK
bBiological Physics Group, School of Physics and Astronomy, The University of Manchester, Manchester, M60 1QD, UK
cCardiovascular Biology Group, Departments of Biochemistry and Physiology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, UK

* Corresponding author. Division of Cardiovascular and Endocrine Sciences, The University of Manchester, Manchester, M13, 9NT. Tel.: +44 161 2751194; fax: +44 161 2751183. Email address: ming.lei{at}manchester.ac.uk

The SCN5A gene encodes specific voltage-dependent Na+ channels abundant in cardiac muscle that open and close at specific stages of cardiac activity in response to voltage change, thereby controlling the magnitude and timecourse of voltage-dependent Na+ currents (iNa) in cardiac muscle cells. Although iNa has been recorded from sinoatrial (SA) node pacemaker cells, its precise role in SA node pacemaker function remains uncertain. This review summarizes recent findings bearing upon: (i) Sinus node dysfunction resulting from genetic mutations in SCN5A; (ii) Sinus node function in the murine cardiac model with targeted disruptions of the SCN5A gene; (iii) Experimental and computational evaluations of the functional roles of iNa in SA node pacemaker function. Taken together, these new observations suggest strong correlations between SCN5A-encoded Na+ channel and SA node pacemaker function.

KEYWORDS SA node; Pacemaker activity; Voltage-dependent Na+ channels

Time for primary review 28 days


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