The slow inward current contributes to the normal electrical and contractile activity of several cardiac and vascular tissues and also may mediate the electrical abnormalities responsible for certain cardiac arrhythmias. The slow inward current differs from the fast inward sodium current in that it is carried primarily by calcium rather than sodium, requires a more positive level of membrane potential to be activated, has slower activation and inactivation kinetics, is responsible for normal depolarization in sinus and atrioventricular (AV) nodal cells and is blocked by a rather specific group of agents that includes verapamil, diltiazem and nifedipine. Recent data suggest that slow-channel openings occur in bursts, separated by silent periods, and that less negative membrane potentials and beta-adrenergic stimulation increase the probability that the channels will open. Inactivation of the channels is associated with a lower probability of channel opening. Slow-channel blocking agents such as verapamil, diltiazem and nifedipine appear to bind to activated, rather than rested, slow channels. Therefore, their effects are more prominent at faster pacing rates and at less negative membrane potentials. Clinically occurring cardiac arrhythmias dependent on the slow inward current include primarily sinus and AV nodal reentry and reciprocating tachycardia in the Wolff-Parkinson-White syndrome when one of the pathways incorporates the AV node. Damaged atrial, ventricular and specialized tissue also can generate slow response-mediated reentry or forms of automaticity that may be clinically important under certain circumstances.