Ion Channel Defects in Cardiac Arrhythmia

Ion Channel Defects in Cardiac Arrhythmia J. Membrane Biol. 170, 181–190 (1999) The Journal of Membrane Biology © Springer-Verlag New York Inc. 1999 Topical Review G.E. Kirsch Rammelkamp Center for Education and Research, MetroHealth Medical Center, Department of Physiology and Biophysics, Case Western Reserve University, 2500 MetroHealth Drive, Cleveland OH 44109, USA Received: 25 March 1999/Revised: 26 April 1999 Introduction waveform of the action potential in unclamped cells, and the surface electrocardiogram (ECG) in vivo are summa- Voltage-gated ion channels initiate and conduct electri- rized in Fig. 1. The initial upstroke of the action poten- cal activity in the heart. The channels open and close in tial (phase 0, Fig. 1B) is driven by a brief surge of inward response to changes in membrane potential, and allow current through Na channels that activate rapidly in re- ionic permeation across the plasmalemma. Because of sponse to pacemaker depolarization (not illustrated) and the diversity of channels that participate in cardiac ex- then close rapidly into an inactivated state even though citability and the complex relationships between gating the cell membrane remains partially depolarized and membrane potential, the functional roles of different throughout phases 1 and 2. The SCN5A gene encodes ion channels have been difficult to determine. The Journal of Membrane Biology Springer Journals

Ion Channel Defects in Cardiac Arrhythmia

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Copyright © Inc. by 1999 Springer-Verlag New York
Life Sciences; Biochemistry, general; Human Physiology
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