Effect of the calcium antagonist nimodipine on contractile responses of isolated canine basilar arteries induced by serotonin, prostaglandin F2 alpha, thrombin, and whole blood.

Nimodipine is a new calcium antagonist that has been advocated as a specific treatment for the cerebral vasospasm accompanying subarachnoid hemorrhage in humans because of reports that it selectively inhibits the constriction of cerebral arteries in vitro. Because calcium antagonists may have specific blocking actions, whereas the origin of vasospasm is likely to be multiplex, the effect of nimodipine on the contractions of isolated canine basilar arteries that are produced by serotonin, prostaglandin F2 alpha, thrombin, and whole blood was studied. The results demonstrate that nimodipine significantly inhibits the contractile responses induced by these diverse agonists whether it is given before or after the agonist. The findings suggest that, in canine cerebral arteries, a common calcium influx channel is involved in the responses elicited by a variety of receptor mechanisms and afford a rationale for the use of nimodipine in the treatment of the cerebral ischemia that often follows cerebral hemorrhage.