Abstract
Ca2+ increases in the heart control both contraction and transcription. To accommodate a short-term increased cardiovascular demand, neurohormonal modulators acting on the cardiac pacemaker and individual myocytes induce an increase in frequency and magnitude of myocyte contraction respectively. Prolonged, enhanced function results in hypertrophic growth of the heart, which is initially also associated with greater Ca2+ signals and cardiac contraction. As a result of disease, however, hypertrophy progresses to a decompensated state and Ca2+ signalling capacity and cardiac output are reduced. Here, the role that Ca2+ plays in the induction of hypertrophy as well as the impact that cardiac hypertrophy and failure has on Ca2+ fluxes will be discussed.