Modification of experimental atherosclerosis by calcium-channel blockers.
The process of atherosclerosis, although not completely understood, is being clarified. A unifying hypothesis holds that the initial event is endothelial injury, followed by platelet aggregation and release reactions. This leads to smooth muscle cell migration into the intima and replication, with subsequent secretion of elastin, collagen and glycosaminoglycans (which binds lipids). Several animal studies have shown that calcium plays an important role in this process. Many drugs with diverse properties can inhibit experimental atherosclerosis. These drugs appear to reduce intracellular calcium. The calcium-channel blockers nifedipine, diltiazem and verapamil, which decrease intracellular calcium, also protect animals from experimental atherosclerosis. The relevance of these animal models to human atherosclerosis is uncertain, and there are very few studies concerning regression of atherosclerosis by interfering with calcium fluxes. Further studies will be needed to clarify these points.
D000818:Animals; D001011:Aorta / Q000473:pathology; D001161:Arteriosclerosis / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D002118:Calcium / Q000502:physiology; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D002648:Child; D004036:Diet, Atherogenic; D004110:Diltiazem / Q000494:pharmacology; D004195:Disease Models, Animal; D006801:Humans; D008251:Macaca; D009543:Nifedipine / Q000494:pharmacology; D011817:Rabbits; D051381:Rats; D014700:Verapamil / Q000494:pharmacology
D002121:Calcium Channel Blockers; D014700:Verapamil; D004110:Diltiazem; D009543:Nifedipine; D002118:Calcium