Electrophysiological effects of Ca antagonists, tetrodotoxin, [Ca]o and [Na]o on myocardium of hibernating chipmunks: possible involvement of Na-Ca exchange mechanism.

The electrophysiological performance of myocardium of hibernating chipmunks was investigated in the presence of Ca antagonists and tetrodotoxin, and the effects of high [Ca]o and low [Na]o were examined. The action potential of the preparations was characterized by the low amplitude of the plateau phase (APp). Ca antagonists, nifedipine (10(-6) M) and nitrendipine (2 X 10(-6) M), did not significantly inhibit this APp or the contraction. These nifedipine-insensitive electromechanical responses were completely abolished by an internal Ca release inhibitor, ryanodine. Both increasing [Ca]o and lowering [Na]o, by replacing Na by lithium or choline, also inhibited APp. Tetrodotoxin (10(-5) M) which markedly inhibited the initial rapid phase of the action potential slightly affected APp. These results suggest that the plateau potential of the present preparations is controlled by a process linked to Ca release from internal stores, most likely the Na-Ca exchange mechanism.