Abstract
Isometric tension and membrane potential were measured to determine the electrophysiological events occurring during anoxia in the isolated canine basilar artery. Anoxia induced transient contractions which were inhibited by the Ca2+-channel inhibitor, diltiazem, and were abolished in Ca2+-free solution. Anoxic contractions were accompanied by membrane depolarizations, which were resistant to diltiazem. When matched contractions were obtained with anoxia and high K+, the level of membrane depolarization was smaller during anoxic contractions. These results support the importance of voltage-dependent Ca2 + influx in the generation of anoxic contractions in the canine basilar artery. However, membrane depolarization does not fully account for these anoxic contractions.