K201 modulates excitation–contraction coupling and spontaneous Ca2+ release in normal adult rabbit ventricular cardiomyocytes

Abstract

K201 modifies E-C coupling in normal cardiomyocytes. A dual inhibitory action on SERCA and RyR2 explains the ability of K201 to suppress spontaneous diastolic Ca(2+) release during Ca(2+) overload without significantly affecting Ca(2+) transient amplitude.