Abstract
The heart is the first formed organ in the developing fetus. During fetal and postnatal development cardiomyocytes become terminally differentiated muscular cells that are connected end to end by gap junctions, allowing concerted contractile activity. The contraction–relaxation cycle of cardiomyocytes is orchestrated by cyclic increases and decreases in intracellular Ca 2+ initiated by depolarization of the sarcolemma and sustained by Ca 2+ release and re-uptake by the sarcoplasmic reticulum. When stressed, cardiomyocytes undergo hypertrophic growth and apoptotic responses in vivo as well as in cell culture models. Such changes predispose to heart failure in the longer term.
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