Calcium ions play an important role in the regulation of heart functions. Calcium ions may enter or leave the myocardial cell through various mechanisms, including several exchange mechanisms and pumps. This review concentrates on the influx of calcium ions through channels in the sarcolemma, resulting in an electric current flow. The calcium current plays an important role in the maintenance of the action potential duration, in the generation of pacemaker activity, and in the initiation of contraction. The calcium current displays both activation and a subsequent inactivation when the membrane potential is changed in a stepwise fashion. Previously, the activation was thought to occur rather slowly, hence the name "slow inward current." Recent evidence suggests that the calcium current occurs much faster and that two types of calcium currents might exist, differing in their selectivity to other ions and in their sensitivity to membrane potential and to drugs. The calcium current is modulated by several factors. Beta-adrenergic stimulation increases the calcium current by increasing the opening probability of the calcium channel. The effects of acetylcholine are less well described. There also exists a class of drugs, called calcium channel blockers (or calcium antagonists) that decrease the flow of calcium ions through calcium channels. It is not quite clear how the calcium current is changed during myocardial ischemia. Factors that may reduce the calcium current during ischemia are the increased extracellular potassium concentration, metabolic inhibition and a decreased ATP level, and acidosis. Raised levels of intracellular cAMP, however, should lead to an increased calcium current.