• H L Roderick, D R Higazi, I Smyrnias, C Fearnley, D Harzheim, and M D Bootman.
• Department of Pharmacology, University of Cambridge, Cambridge CB2 1PD, U.K. Llewelyn.roderick@bbsrc.ac.uk
• Biochem. Soc. Trans. 2007 Nov 1; 35 (Pt 5): 957-61.

AbstractCa(2+) 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 Ca(2+) signals and cardiac contraction. As a result of disease, however, hypertrophy progresses to a decompensated state and Ca(2+) signalling capacity and cardiac output are reduced. Here, the role that Ca(2+) plays in the induction of hypertrophy as well as the impact that cardiac hypertrophy and failure has on Ca(2+) fluxes will be discussed.

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