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Na/Ca Exchange and Cardiac Ventricular Arrhythmias

2007; Wiley; Volume: 1099; Issue: 1 Linguagem: Inglês

10.1196/annals.1387.066

1749-6632

KARIN R. SIPIDO, Virginie Bito, Gudrun Antoons, Paul G.A. Volders, Marc A. Vos,

Neuroscience and Neuropharmacology Research

Abstract: Ventricular arrhythmias are a major cause of death in cardiovascular disease. Ca 2+ removal from the cell by the electrogenic Na/Ca exchanger is essential for the Ca 2+ flux balance during excitation–contraction coupling but also contributes to the electrical events. “Classic” views on the exchanger in arrhythmias include its well‐recognized role as depolarizing current underlying delayed afterdepolarizations (DADs) during spontaneous Ca 2+ release and the alterations in expression in certain forms of cardiac hypertrophy and heart failure. “Novel” views relate to more subtle roles for the exchanger in arrhythmias. Na/Ca exchange function in disease could be modulated indirectly, through phosphorylation or anchoring proteins. Ongoing studies relate Na/Ca exchange to variability in action potential duration (APD) and early afterdepolarizations (EADs) in a dog model of cardiac hypertrophy and arrhythmias. Further research on drugs that target Na/Ca exchange will have to carefully examine the effects on Ca 2+ balance.