Control of descending vasa recta pericyte membrane potential by angiotensin II.
Control of descending vasa recta pericyte membrane potential by angiotensin II.
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血管紧张素 II 对降直血管周细胞膜电位的控制。
DOI：
10.1152/ajprenal.00306.2001
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发表时间：
2002
期刊：
影响因子：
--
通讯作者：
Huang,JamesM-C
中科院分区：
文献类型：
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作者：
Pallone,ThomasL;Huang,JamesM-C
使用制霉菌素穿孔膜片全细胞记录，我们研究了Cl−电导在ANG II调节外髓降直小血管（OMDVR）周细胞膜电位（PRM）中的作用。ANG II（10− 11至10− 7 M）在较低浓度下持续使OMDVR去极化并诱导OMDVR振荡。Cl−通道阻断剂蒽-9-脱羧酸酯（1 mM）和尼氟灭酸（10 μM）使静息周细胞超极化，并使ANG II处理的周细胞复极化。在电压钳实验中，ANG II处理的周细胞表现出缓慢的激活电流，这些电流几乎被尼氟灭酸（10 μM）处理或去除细胞外Ca 2+所消除。当细胞外Cl−浓度分别为152和34 mM时，这些电流分别在-31和-10 mV时逆转。在周细胞保持在-70 mV时，有时会观察到振荡的内向电流;反转电位也会随着细胞外Cl−浓度的变化而变化。我们的结论是，ANG II激活OMDVR周细胞中的Ca 2+依赖性Cl−电导，以诱导膜去极化和膜振荡。
Using nystatin perforated-patch whole cell recording, we investigated the role of Cl−conductance in the modulation of outer medullary descending vasa recta (OMDVR) pericyte membrane potential (Ψm) by ANG II. ANG II (10−11to 10−7M) consistently depolarized OMDVR and induced Ψm oscillations at lower concentrations. The Cl−channel blockers anthracene-9-decarboxylate (1 mM) and niflumic acid (10 μM) hyperpolarized resting pericytes and repolarized ANG II-treated pericytes. In voltage-clamp experiments, ANG II-treated pericytes exhibited slowly activating currents that were nearly eliminated by treatment with niflumic acid (10 μM) or removal of extracellular Ca2+. Those currents reversed at −31 and −10 mV when extracellular Cl−concentration was 152 and 34 mM, respectively. In pericytes held at −70 mV, oscillating inward currents were sometimes observed; the reversal potential also shifted with extracellular Cl−concentration. We conclude that ANG II activates a Ca2+-dependent Cl−conductance in OMDVR pericytes to induce membrane depolarization and Ψm oscillations.