Cellular calcium metabolism: activation and antagonism.
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.
D000494:Allosteric Regulation; D001249:Asthma / Q000378:metabolism; D001665:Binding Sites; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000378:metabolism* / Q000494:pharmacology; D002462:Cell Membrane / Q000378:metabolism; D055598:Chemical Phenomena; D002621:Chemistry; D004095:Dihydropyridines; D006801:Humans; D007473:Ion Channels / Q000187:drug effects / Q000378:metabolism*; D009130:Muscle, Smooth / Q000378:metabolism; D010743:Phospholipids / Q000378:metabolism; D011725:Pyridines / Q000378:metabolism
D002121:Calcium Channel Blockers; D004095:Dihydropyridines; D007473:Ion Channels; D010743:Phospholipids; D011725:Pyridines; C038806:1,4-dihydropyridine; D002118:Calcium