Bennett P B, Kass R, Begenisich T
Department of Physiology, University of Rochester School of Medicine and Dentistry, New York 14642.
Biophys J. 1989 Apr;55(4):731-8. doi: 10.1016/S0006-3495(89)82872-3.
We have studied the large increase in macroscopic potassium channel current caused by catecholamines in mammalian cardiac cells. An increase in macroscopic K current could result from either an increase in the single-channel current or by an increase in the number of channels that are open. Therefore, we have measured nonstationary potassium current fluctuations under voltage clamp conditions to determine whether norepinephrine increases the current through this channel. The single-channel current (at a potential of -30 mV in 4 mM external [K]) was estimated to be 3.7 pA and was not altered by concentrations of norepinephrine up to 2 microM. The spectral density of the current fluctuations were fitted well by a sum of 2 Lorentzians with corner frequencies that correspond with the measured time constants for deactivation of the macroscopic K current tails. We conclude that the increase in macroscopic K current caused by norepinephrine in these cells is not the result of an increase in single-channel conductance and therefore must involve an increase in the number of open K channels.
我们研究了儿茶酚胺引起的哺乳动物心肌细胞中宏观钾通道电流的大幅增加。宏观钾电流的增加可能是由于单通道电流增加或开放通道数量增加所致。因此，我们在电压钳制条件下测量了非平稳钾电流波动，以确定去甲肾上腺素是否增加了通过该通道的电流。单通道电流（在4 mM外部[K]中-30 mV的电位下）估计为3.7 pA，并且在高达2 microM的去甲肾上腺素浓度下未发生改变。电流波动的频谱密度通过2个洛伦兹函数的总和得到了很好的拟合，其转折频率与测量的宏观钾电流尾电流失活时间常数相对应。我们得出结论，去甲肾上腺素在这些细胞中引起的宏观钾电流增加不是单通道电导增加的结果，因此必然涉及开放钾通道数量的增加。
