抄録
Action potential waveform is surely the most important issue for discussing electrical activities in the heart. However in the mouse, the waveform of cardiac action potentials is still controversial and large variations are observed among the reports. Here, I aim to confirm physiological waveform of ventricular action potentials of the mouse, and also to reveal the cellular mechanism that underlies those waveform variations. For this purpose, I recorded action potentials from whole-cell clamped adult mouse ventricular myocytes, with the aid of a novel concentration-jump device that rapidly switches between superfusates. When being recorded with conventional whole-cell patch, the action potentials had a plateau that peaked at around -30 mV. This waveform is considered to be physiological because the same action potentials were also recorded with nystatin-perforated patch. On the other hand, the plateau was abolished when BAPTA (2 mM) or ryanodine (20 uM) was included in the electrodes, indicating that the development of the plateau demands the presence of [Ca2+]i transients. The plateau was abolished by KB-R7943 (5 uM), a blocker of the Na/Ca exchanger, or by temporarily substituting extracellular Na with Li during the action potential, indicating a mandatory involvement of the Na/Ca exchange current in the development of the plateau. These results indicate that the variation in the action potential waveform is closely related to the variation in [Ca2+]i transient, via the operation of Na/Ca exchange that provides inward current during the [Ca2+]i transient. [Jpn J Physiol 54 Suppl:S107 (2004)]
