Central to controlling intracellular calcium concentration ([Ca(2+)](i)) are a 
number of Ca(2+) transporters and channels with the L-type Ca(2+) channel, 
Na(+)-Ca(2+) exchanger and sarcoplasmic reticulum Ca(2+)-ATPase (SERCA) being of 
particular note in the heart. This review concentrates on the regulation of 
[Ca(2+)](i) in cardiac muscle and the homeostatic mechanisms employed to ensure 
that the heart can operate under steady-state conditions on a beat by beat 
basis. To this end we discuss the relative importance of various sources and 
sinks of Ca(2+) responsible for initiating contraction and relaxation in cardiac 
myocytes and how these can be manipulated to regulate the Ca(2+) content of the 
major Ca(2+) store, the sarcoplasmic reticulum (SR). We will present a simple 
feedback system detailing how such control can be achieved and highlight how 
small perturbations to the steady-state operation of the feedback loop can be 
both beneficial physiologically and underlie changes in systolic Ca(2+) in 
ageing and heart disease. In addition to manipulating the amplitude of the 
normal systolic Ca(2+) transient, the tight regulation of SR Ca(2+) content is 
also required to prevent the abnormal, spontaneous or diastolic release of 
Ca(2+) from the SR. Such diastolic events are a major factor contributing to the 
genesis of cardiac arrhythmias in disease situations and in recently identified 
familial mutations in the SR Ca(2+) release channel (ryanodine receptor, RyR). 
How such diastolic release arises and potential mechanisms for controlling this 
will be discussed.