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目的:研究HERG钾通道在细胞容量调节中的作用,并探讨其作用机制。方法:全部试验应用稳定转染HERG-HEK293细胞和HEK293细胞。应用全细胞膜片钳技术记录HERG钾电流。结果:1当HERG-HEK293细胞处于低渗状态,指令电压为0 mV时,Istep增加60%(n=12,P<0.05);如指令电压为+30 mV,Itail增加72.1%(n=11,P<0.01),增大的HERG电流可被特异性HERG钾电流阻断剂Cisapride(100nM)抑制,Istep被抑制97.2%(n=6,P<0.01),Itail被抑制174.1%(n=6,P<0.01)。2在低渗状态,指令电压为0 mV时,容量调节性氯通道阻断剂尼氟灭酸(NFA,10 nmol/L)使Istep抑制46.2%(n=12,P<0.01),Itail抑制48.5%(n=11,P<0.01);给以容量调节性氯通道阻断剂DIDS 100μmol/L时,Istep抑制45.9%(n=12,P<0.01),Itail抑制51.1%(n=11,P<0.01)。结论:HERG通道部分参与调节性细胞容量下降过程。其参与的细胞容量调节与容量调节性氯通道的激活相伴随。
AIM: To investigate the role of HERG potassium channel in the regulation of cell volume and its mechanism of action. METHODS: HERG-293 cells and HEK293 cells were stably transfected in all experiments. HERG potassium currents were recorded using whole-cell patch clamp techniques. RESULTS: Istep was increased by 60% (n = 12, P <0.05) when HERG-HEK293 cells were hypotonic at a command voltage of 0 mV and increased by 72.1% (n = 11) at a command voltage of +30 mV , P <0.01), increased HERG currents were inhibited by a specific HERG potassium current blocker Cisapride (100 nM), Istep was inhibited by 97.2% (n = 6, 6, P <0.01). 2 In hypotonic conditions, the volume-regulated chloride channel blocker niflumic acid (NFA, 10 nmol / L) inhibited Istep by 46.2% (n = 12, P <0.01) 48.5% (n = 11, P <0.01). Istep was inhibited by 45.9% (n = 12, P <0.01) and Itail was inhibited by 51.1% (n = 11 , P <0.01). Conclusions: The HERG channel is partially involved in the process of regulatory cell capacity decline. Its involvement in the regulation of cell volume and capacity-regulated chloride channel is accompanied.