Study on the regulation of Na/Ca exchange in isolated cardiac myocytes.

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Ca^<2+> influx via reverse-mode Na^+/Ca^<2+> exchanger was responsible for the Na^+ withdrawal Ca^<2+> transient (SWCT), which is caused by low Na^+ perfusion in isolated cardiac myocytes. The SWCT was inhibited during metabolic inhibition despite an increase in [Na^+] while it was increased on the washout of metabolic inhibitor. It was suggested that Na^+/Ca^<2+> exchanger was inhibited during metabolic inhibition in spite of an increase in electrical gradient of Na^+.KB-R7943, a specific inhibitor of reverse-mode Na^+ /Ca^<2+> exchanger, did not change the cellular contraction and Ca^<2+> transient in steady-state condition. KB-R7943 also did not change the Ca^<2+> content in the sarcoplasmic reticulum, post-rest potentiation of contraction and Ca^<2+> transient, and the action potential. On the other hand, KB-R7943 inhibited an increase in diastolic [Ca2^<2+>]i and spontaneous Ca^<2+> oscillation in myocytes in which [Na^+]i was increased by strophanthidin while it did not inhibit the positive inotropic effect of strophanthidin. In addition, KB-R7943 reduced the incidence of reoxygenation-induced arrhythmias and facilitated the recovery of contraction after reoxygenation. These results suggested that Ca^<2+> influx via reverse-mode Na^+/Ca^<2+> exchanger dose not have the significant roles in normal excitation-contraction coupling and positive inotropy of cardiac glycoside while it is related to arrhythmogenesis and Ca^<2+> overload in myocytes in which [Na^<2+>]i was elevated by cardiac glycoside and metabolic inhibition.