We investigate the impact of stress-induced transcriptional changes on cardiac function at the level of sarcolemmal Ca²⁺-handling proteins and Ca²⁺ channels of the sarcoplasmic reticulum. Novel pharmacological compounds are tested for their capability of reversing pathological remodeling at the cellular level.

_{Cardiac excitation-contraction coupling and Ca²⁺ current properties. Left: Ca²⁺-induced Ca²⁺ release in adult ventricular cardiomyocytes. L-type Ca²⁺ currents are elicited by depolarization to different membrane potentials. In parallel, cytosolic Ca²⁺ levels are monitored in the line-scan mode using a Ca²⁺-sensitive fluorescent indicator. Right: activation and inactivation curves of the L-type Ca²⁺ channel under control conditions (black) and in the presence of two compounds with different effects on the channel kinetics (red, blue).}