The hemodynamic properties of the calcium entry-blocking agents result principally from the inhibition of transcellular calcium flux in the myocardium and in vascular smooth muscle. The composite effect(s) of these compounds on cardiovascular function derive from a complex interplay between their direct (myocardial depression) and indirect (afterload reduction by peripheral arterial vasodilation, reflex sympathetic stimulation) actions. While qualitatively similar, the currently available agents (diltiazem, nifedipine, verapamil) differ considerably in relative negative inotropic, vasodilator, and reflex properties. The hemodynamic actions of a particular calcium blocker also critically depend on the baseline cardiocirculatory status. Current information regarding these issues from basic and clinical investigations is reviewed.