Pharmacology of nimodipine, a calcium antagonist with preferential cerebrovascular activity.
In isolated vessels in vitro nimodipine inhibits spasms induced by depolarization independently of the vessel's origin. The spasms induced by spasmogenic agonists such as serotonin, catecholamines, histamine, thromboxane, or whole blood are inhibited only in the cerebral vessels and not in the peripheral vessels. In vivo, nimodipine inhibits cerebrovascular spasms and brain damage in acute and chronic animal experiments. In chronic studies on stroke-prone, spontaneously hypertensive rats, nimodipine prevents cerebral tissue damage and prolongs the survival time without affecting the high blood pressure. Nimodipine inhibits the transmembraneous calcium influx in the smooth muscle cells of the cerebral vessels and thus prevents cerebral hypoperfusion after spasmogenic stimulation. In chronic cerebrovascular stress nimodipine prevents harmful calcium overloading and thus ensures the integrity of the cerebral parenchyma.
D000818:Animals; D000959:Antihypertensive Agents; D001808:Blood Vessels / Q000187:drug effects; D001921:Brain / Q000098:blood supply; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D004285:Dogs; D002546:Ischemic Attack, Transient / Q000188:drug therapy; D009131:Muscle, Smooth, Vascular / Q000187:drug effects; D009539:Nicotinic Acids / Q000494:pharmacology* / Q000627:therapeutic use; D009553:Nimodipine; D011817:Rabbits; D051381:Rats; D011918:Rats, Inbred SHR; D014665:Vasodilator Agents / Q000494:pharmacology*
D000959:Antihypertensive Agents; D002121:Calcium Channel Blockers; D009539:Nicotinic Acids; D014665:Vasodilator Agents; D009553:Nimodipine