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Computational evaluation of the roles of Na⁺ current, i_Na, and cell death in cardiac pacemaking and driving

¹Biological Physics Group, School of Physics and Astronomy and ²Division of Cardiovascular and Endocrine Sciences, The University of Manchester, Manchester, United Kingdom; ³College of Information Science and Engineering, Northeastern University, Shenyang, China; and ⁴Institute of Membrane and Systems Biology, The University of Leeds, Leeds, United Kingdom

Submitted 18 October 2005 ; accepted in final form 27 July 2006

Voltage-dependent sodium (Na⁺) channels are heterogeneously distributed through the pacemaker of the heart, the sinoatrial node (SA node). The measured sodium channel current (i_Na) density is higher in the periphery but low or zero in the center of the SA node. The functional roles of i_Na in initiation and conduction of cardiac pacemaker activity remain uncertain. We evaluated the functional roles of i_Na by computer modeling. A gradient model of the intact SA node and atrium of the rabbit heart was developed that incorporates both heterogeneities of the SA node electrophysiology and histological structure. Our computations show that a large i_Na in the periphery helps the SA node to drive the atrial muscle. Removal i_Na from the SA node slows down the pacemaking rate and increases the sinoatrial node-atrium conduction time. In some cases, reduction of the SA node i_Na results in impairment of impulse initiation and conduction that leads to the SA node-atrium conduction exit block. Decrease in active SA node cell population has similar effects. Combined actions of reduced cell population and removal of i_Na from the SA node have greater impacts on weakening the ability of the SA node to pace and drive the atrium.

sodium current; sinoatrial node; aging; dysfunction; conduction block; computer simulation

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