The plateau potential in the myocardium of hibernating chipmunks appears to be controlled by calcium release from internal stores, likely involving the Na-Ca exchange mechanism.
Findings from hibernating chipmunks warrant no change in clinical calcium antagonist use; leaves open the role of internal stores and Na-Ca exchange in human myocardium.
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.
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Noriaki Kondo (1987) studied this question.
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