Abstract
The role of Ca2+ as a mediator of many cellular responses, including stimulus-secretion and excitation-contraction coupling, is reviewed. Pathways of Ca2+ mobilization are discussed in terms of both intracellular and plasmalemmal processes. The extent to which specific antagonists exist, active at these several sites, is noted, with particular emphasis on the clinically available Ca2+ channel antagonists, including verapamil, nifedipine, and diltiazem.