Nonstationary fluctuation analysis of the delayed rectifier K channel in cardiac Purkinje fibers. Actions of norepinephrine on single-channel current.

Nonstationary fluctuation analysis of the delayed rectifier K channel in cardiac Purkinje fibers. Actions of norepinephrine on single-channel current.
复制标题

心脏浦肯野纤维延迟整流 K 通道的非平稳波动分析。

DOI:
10.1016/s0006-3495(89)82872-3
复制
发表时间:
1989
影响因子:
3.4
通讯作者:
Begenisich,T
Begenisich,T
中科院分区:
生物学3区
文献类型:
--
作者:
Bennett,PB;Kass,R;Begenisich,T

文献摘要

被引文献

相似文献

我们研究了儿茶酚胺在哺乳动物心脏细胞中引起的宏观钾通道电流的大幅增加。宏观K电流的增加可能是由单通道电流的增加或打开通道数量的增加引起的。因此,我们在电压箝位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4mm外部[K]中- 30mv的电位)估计为3.7 pA,并且不受高达2微米的去甲肾上腺素浓度的影响。通过角频率与宏观K电流尾失活时间常数相对应的2个洛伦兹量的和,可以很好地拟合出电流波动的谱密度。我们得出结论,这些细胞中去甲肾上腺素引起的宏观K电流的增加不是单通道电导增加的结果,因此必须涉及开放K通道数量的增加。
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.