L-type Ca(2+) current in ventricular cardiomyocytes

Abstract

L-type Ca(2+) channels are mediators of Ca(2+) influx and the regulatory events accompanying it and are pivotal in the function and dysfunction of ventricular cardiac myocytes. L-type Ca(2+) channels are located in sarcolemma, including the T-tubules facing the sarcoplasmic reticulum junction, and are activated by membrane depolarization, but intracellular Ca(2+)-dependent inactivation limits Ca(2+) influx during action potential. I(CaL) is important in heart function because it triggers excitation-contraction coupling, modulates action potential shape and is involved in cardiac arrhythmia. L-type Ca(2+) channels are multi-subunit complexes that interact with several molecules involved in their regulations, notably by beta-adrenergic signaling. The present review highlights some of the recent findings on L-type Ca(2+) channel function, regulation, and alteration in acquired pathologies such as cardiac hypertrophy, heart failure and diabetic cardiomyopathy, as well as in inherited arrhythmic cardiac diseases such as Timothy and Brugada syndromes.