Kanazirska M V, Vassilev P M, Quinn S J, Tillotson D L, Williams G H
Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts.
Am J Physiol. 1992 Oct;263(4 Pt 1):E760-5. doi: 10.1152/ajpendo.1992.263.4.E760.
The effects of angiotensin II (ANG II) on single K+ channels were studied in rat and bovine adrenal zona glomerulosa (ZG) cells, using the patch-clamp technique. ANG II (0.1-10 nM) induced substantial inhibition of inward rectifier and delayed rectifier K+ channel activities in rat and bovine ZG cells. Analysis of single-channel activities showed that the ANG II-induced channel-blocking effect involved reductions in the probability of the open state (Po) and the mean open time. The changes in these channel parameters occurred at all test voltages, indicating that the effect of ANG II was voltage independent. ANG II could not interact directly with the extracellular sides of the membranes in these experiments using cell-attached patches. Therefore, the effect of ANG II on K+ channels must occur through an indirect cytosolic transduction pathway. The ANG II-induced block of K+ channels will result in membrane depolarization, which may activate voltage-dependent Ca2+ channels, thereby increasing cytosolic free Ca2+ and stimulating aldosterone secretion. These channel-modulating actions of ANG II may be an important step in the initial sequence of events underlying its transduction mechanism.
采用膜片钳技术，研究了血管紧张素II（ANG II）对大鼠和牛肾上腺球状带（ZG）细胞中单个钾离子通道的影响。ANG II（0.1 - 10 nM）可显著抑制大鼠和牛ZG细胞中的内向整流钾离子通道和延迟整流钾离子通道活性。单通道活性分析表明，ANG II诱导的通道阻断效应涉及开放态概率（Po）和平均开放时间的降低。这些通道参数的变化在所有测试电压下均会出现，表明ANG II的作用与电压无关。在使用细胞贴附式膜片的这些实验中，ANG II无法直接与细胞膜的胞外侧相互作用。因此，ANG II对钾离子通道的作用必定通过间接的胞质转导途径发生。ANG II诱导的钾离子通道阻断将导致膜去极化，这可能会激活电压依赖性钙离子通道，从而增加胞质游离钙离子并刺激醛固酮分泌。ANG II的这些通道调节作用可能是其转导机制初始事件序列中的重要一步。
