Our team examines cardiac Ca2+ signaling and ECC on the cellular and subcellular level. Amplitude, time-course and spatio-temporal features of Ca2+ signals govern the force generated by the heart during each beat. For experimental studies on isolated cardiomyocytes we apply a combination of biophysical techniques: laser-scanning confocal microscopic Ca2+ imaging, UV-laser flash and two-photon excitation photolysis of caged compounds and the patch-clamp technique. Properties of elementary Ca2+ signaling events, the Ca2+ sparks, are examined. The role of ion channels (L-type Ca2+ channels, sarcoplasmic reticulum (SR) Ca2+ release channels (ryanodine receptors)) and ion transporters (Na+-Ca2+ exchanger, SR Ca2+ pump) is analyzed in the process of Ca2+ signaling. Abnormal Ca2+ signals occur during many cardiac pathologies, can contribute to a weak heart beat in disease, and can cause arrhythmias. In collaboration with partner laboratories we therefore also investigate basic features of ECC and Ca2+ signaling in several models relevant for human cardiac disease.