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

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