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.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002118:Calcium / Q000502:physiology*; D002712:Chlorides / Q000494:pharmacology; D005260:Female; D006321:Heart / Q000502:physiology*; D006605:Hibernation; D066298:In Vitro Techniques; D008094:Lithium / Q000494:pharmacology; D018021:Lithium Chloride; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects; D009543:Nifedipine / Q000494:pharmacology; D012433:Ryanodine / Q000494:pharmacology; D012589:Sciuridae / Q000502:physiology*; D012964:Sodium / Q000502:physiology; D013779:Tetrodotoxin / Q000494:pharmacology
D002712:Chlorides; D012433:Ryanodine; D013779:Tetrodotoxin; D008094:Lithium; D012964:Sodium; D018021:Lithium Chloride; D009543:Nifedipine; D002118:Calcium