抄録
HL-1 cells are cardiac myocytes derived from the atria of a transgenic mouse expressing the simian virus 40 (SV40) large T antigen and retains the adult differentiated cardiomyocyte phenotype. The present study was designed to characterize the K+ channel current in HL-1 cells using the whole-cell patch-clamp methods. In the presence of 0.4 μM nisoldipine, depolarizing voltage steps applied from a holding potential of –50 mV elicited the time-dependent outward current, followed by the decaying outward tail current upon return to the holding potential. The amplitude of the outward current was increased with depolarizations up to 0 mV but was then progressively decreased with further depolarizations. E-4031 (5 μM) or dofetilide (1 μM) almost totally abolished the time-dependent outward current as well as the tail current, suggesting that the outward current activated by depolarizations in HL-1 cells was mostly attributable to the rapidly activating delayed rectifier K+ current (IKr). The inhibitory effect of E-4031 and dofetilide was concentration-dependent with IC50 of 21.1 and 15.1 nM, respectively. IKr in HL-1 cells was activated in response to membrane depolarization with V1/2 of –20.4 mV. IKr in HL-1 cells also exhibited voltage-dependent inactivation during membrane depolarization with V1/2 of –47.5 mV. Thus, properties of IKr in HL-1 cells are comparable to those of IKr in native mammalian cardiac cells and HL-1 cells provide a suitable experimental model for studies of native cardiac IKr. [Jpn J Physiol 54 Suppl:S127 (2004)]
