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Cardiovascular Research 2007 75(3):455-456; doi:10.1016/j.cardiores.2007.06.009
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Copyright © 2007, European Society of Cardiology

Cardiac sodium channels: Dysregulation meets myocardial failure

Eric Schulze-Bahr1,*

Department of Cardiology and Angiology, University Hospital Münster, the Leibniz-Institute for Arteriosclerosis Research (LIFA) at the University of Münster, the Centre for Interdisciplinary Clinical Research (IZKF) of the University Hospital Münster, Germany

* Tel.: +49 251 83 529 82; fax: +49 251 83 575 70. Eric.Schulze-Bahr@ukmuenster.de http://www.medc.uni-muenster.de

Received 3 June 2007; accepted 15 June 2007

The first 10% of the full text of this article appears below.

See article by Hesse et al. [12] (pages 498–509) in this issue.

Within the orchestra of cardiac ion channels, voltage–gated Na+ channels have a key function in the determination of the amplitude and slope of the action potential upstroke. Both are important in the control of impulse conduction velocity and maintenance of appropriate waves of excitation through the working myocardium. The main ({alpha}-) subunit of the cardiac sodium channel is encoded by the SCN5A (Nav1.5) gene, and the INa current mediated is responsible for the membrane depolarization. Fast inactivation of sodium . . . [Full Text of this Article]


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