Ganfornina M D, López-Barneo J
Departamento de Fisiología y Biofísica, Facultad de Medicina, Universidad de Sevilla, Spain.
J Gen Physiol. 1992 Sep;100(3):401-26. doi: 10.1085/jgp.100.3.401.
Single K+ channel currents were recorded in excised membrane patches from dispersed chemoreceptor cells of the rabbit carotid body under conditions that abolish current flow through Na+ and Ca2+ channels. We have found three classes of voltage-gated K+ channels that differ in their single-channel conductance (gamma), dependence on internal Ca2+ (Ca2+i), and sensitivity to changes in O2 tension (PO2). Ca(2+)-activated K+ channels (KCa channels) with gamma approximately 210 pS in symmetrical K+ solutions were observed when [Ca2+]i was greater than 0.1 microM. Small conductance channels with gamma = 16 pS were not affected by [Ca2+]i and they exhibited slow activation and inactivation time courses. In these two channel types open probability (P(open)) was unaffected when exposed to normoxic (PO2 = 140 mmHg) or hypoxic (PO2 approximately 5-10 mmHg) external solutions. A third channel type (referred to as KO2 channel), having an intermediate gamma(approximately 40 pS), was the most frequently recorded. KO2 channels are steeply voltage dependent and not affected by [Ca2+]i, they inactivate almost completely in less than 500 ms, and their P(open) reversibly decreases upon exposure to low PO2. The effect of low PO2 is voltage dependent, being more pronounced at moderately depolarized voltages. At 0 mV, for example, P(open) diminishes to approximately 40% of the control value. The time course of ensemble current averages of KO2 channels is remarkably similar to that of the O2-sensitive K+ current. In addition, ensemble average and macroscopic K+ currents are affected similarly by low PO2. These observations strongly suggest that KO2 channels are the main contributors to the macroscopic K+ current of glomus cells. The reversible inhibition of KO2 channel activity by low PO2 does not desensitize and is not related to the presence of F-, ATP, and GTP-gamma-S at the internal face of the membrane. These results indicate that KO2 channels confer upon glomus cells their unique chemoreceptor properties and that the O2-K+ channel interaction occurs either directly or through an O2 sensor intrinsic to the plasma membrane closely associated with the channel molecule.
在去除通过钠通道和钙通道电流的条件下，记录了家兔颈动脉体分散化学感受细胞的膜片上的单个钾通道电流。我们发现了三类电压门控钾通道，它们在单通道电导（γ）、对胞内钙（Ca₂⁺i）的依赖性以及对氧分压（PO₂）变化的敏感性方面存在差异。当Ca₂⁺i大于0.1微摩尔时，在对称钾溶液中观察到单通道电导γ约为210皮秒的钙激活钾通道（KCa通道）。电导γ = 16皮秒的小电导通道不受Ca₂⁺i影响，且表现出缓慢的激活和失活时间进程。在这两种通道类型中，当暴露于常氧（PO₂ = 140 mmHg）或低氧（PO₂约为5 - 10 mmHg）的外部溶液时，开放概率（P(open)）不受影响。第三种通道类型（称为KO₂通道），其γ介于中间（约40皮秒），是记录最频繁的。KO₂通道强烈依赖电压且不受Ca₂⁺i影响，它们在不到500毫秒内几乎完全失活，并且在暴露于低PO₂时其P(open)可逆性降低。低PO₂的影响依赖电压，在适度去极化电压下更明显。例如，在0 mV时，P(open)降至对照值的约40%。KO₂通道的整体电流平均值的时间进程与氧敏感钾电流的时间进程非常相似。此外，低PO₂对整体平均值和宏观钾电流的影响相似。这些观察结果强烈表明，KO₂通道是球细胞宏观钾电流的主要贡献者。低PO₂对KO₂通道活性的可逆抑制不会脱敏，且与膜内表面的氟离子、ATP和鸟苷三磷酸γ - S的存在无关。这些结果表明，KO₂通道赋予球细胞其独特的化学感受特性，并且氧 - 钾通道相互作用要么直接发生，要么通过与通道分子紧密相关的质膜固有氧传感器发生。
