Yatani A, Brown A M, Akaike N
J Membr Biol. 1984;78(2):163-8. doi: 10.1007/BF01869203.
Effects of extracellular pH on the sodium current (INa) of single rat ventricular cells were examined under conditions of voltage clamp and internal perfusion. In this way, pHi was controlled while pHo was changed. The combined suction pipette-microelectrode method was used. The suction pipette passed current and perfused the cell's interior; the microelectrode measured membrane potential. Increasing extracellular H+ depressed INa and slowed inactivation. The current-voltage curves for INa were shifted to positive and negative potentials at low and high pHo, respectively. Similar potential shifts were observed in both the conductance voltage curve and the steady-state inactivation voltage curve (h infinity). Conduction was also depressed at low pHo. The shifts were probably due to surface charge effects, while the impaired conduction was probably due to protonation of a site in the Na channel.
在电压钳制和内部灌注条件下,研究了细胞外pH对单个大鼠心室肌细胞钠电流(INa)的影响。通过这种方式,在改变细胞外pH(pHo)的同时控制细胞内pH(pHi)。采用吸液管-微电极联合方法。吸液管通过电流并灌注细胞内部;微电极测量膜电位。细胞外H+浓度增加会抑制INa并减慢失活过程。在低pHo和高pHo条件下,INa的电流-电压曲线分别向正向和负向电位移动。在电导电压曲线和稳态失活电压曲线(h无穷大)中均观察到类似的电位移动。在低pHo时传导也受到抑制。这些电位移动可能是由于表面电荷效应引起的,而传导受损可能是由于Na通道中一个位点的质子化所致。