Na/Ca exchange and cardiac ventricular arrhythmias.
Ventricular arrhythmias are a major cause of death in cardiovascular disease. Ca2+ removal from the cell by the electrogenic Na/Ca exchanger is essential for the Ca2+ 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 Ca2+ 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 Ca2+ balance.
Sipido
Karin R
KR
Laboratory of Experimental Cardiology, KUL, Campus Gasthuisberg O/N1, 704, Herestraat 49, B-3000 Leuven, Belgium. Karin.Sipido@med.kuleuven.be
Bito
V
V
Antoons
G
G
Volders
Paul G
PG
Vos
Marc A
MA
D001145:Arrhythmias, Cardiac / Q000503:physiopathology*; D006352:Heart Ventricles / Q000503:physiopathology*; D006801:Humans; D019831:Sodium-Calcium Exchanger / Q000502:physiology*
D019831:Sodium-Calcium Exchanger