Cardiac contraction is initiated by an increase of cytoplasmic calcium concentration ([Ca2+]i); relaxation requires that [Ca2+]i be reduced to control levels. Most of the calcium is released from the sarcoplasmic reticulum (SR) through a specialized released channel, the ryanodine receptor (RyR). The probability that the RyR is open is increased by a rise in [Ca2+]i. This therefore leads to the mechanism of calcium-induced Ca release in which the entry of a small amount of Ca into the cell through the sarcolemmal L-type Ca channels triggers the release of much more Ca through the RyR. Relaxation occurs via Ca reuptake into the SR and pumping out of the cell. There are three potential control points at which the size of the systolic Ca transient can be altered: (1) the amplitude of the L-type Ca current; (2) the properties of the RyR, in particular the relationship between [Ca2+]i and channel opening; (3) the Ca content of the SR. I will discuss the importance of these various control points. A further important topic concerns the fact that when the cell and therefore the SR is excessively loaded with calcium then the SR releases Ca spontaneously. This triggers arrhythmias and ways of avoiding this will be discussed.
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