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细胞膜拉伸可激活动脉平滑肌细胞中的中电导钙激活钾通道。

Cell membrane stretch activates intermediate-conductance Ca2+-activated K+ channels in arterial smooth muscle cells.

作者信息

Hayabuchi Yasunobu, Nakaya Yutaka, Mawatari Kazuaki, Inoue Miki, Sakata Miho, Kagami Shoji

机构信息

Department of Pediatrics, School of Medicine, University of Tokushima, 3-18-15 Kuramoto-cho, Tokushima, 770-8503, Japan.

出版信息

Heart Vessels. 2011 Jan;26(1):91-100. doi: 10.1007/s00380-010-0025-0. Epub 2010 Nov 10.

Abstract

The aim of this study is to determine the signal transduction of membrane stretch on intermediate-conductance Ca(2+)-activated K(+) (IKca) channels in rat aorta smooth muscle cells using the patch-clamp technique. To stretch the cell membrane, both suction to the rear end of patch pipette and hypotonic shock were used. In cell-attached and inside-out patch configurations, the open probability of IKca channels increased when 20- to 45-mmHg suction was applied. Hyposmotic swelling efficiently increased IKca channel current. When the Ca(2+)-free solution was superfused, the activation of IKca current by the hyposmotic swelling was reduced. Furthermore, gadolinium (Gd(3+)) attenuated the activation of IKca channels induced by hyposmotic swelling, whereas nicardipine did not. In the experiments with Ca(2+)-free bath solution, pretreatment with GF109203X, a protein kinase C (PKC) inhibitor, completely abolished the stretch-induced activation of IKca currents. The stretch-induced activation of IKca channels was strongly inhibited by cytochalasin D, indicating a role for the F-actin in modulation of IKca channels by changes in cell stretching. These data suggest that cell membrane stretch activates IKca channels. In addition, the activation is associated with extracellular Ca(2+) influx through stretch-activated nonselective cation channels, and is also modulated by the F-actin cytoskeleton and the activation of PKC.

摘要

本研究的目的是使用膜片钳技术确定大鼠主动脉平滑肌细胞中膜拉伸对中间电导钙激活钾(IKca)通道的信号转导。为了拉伸细胞膜,采用了对膜片吸管后端施加吸力和低渗休克两种方法。在细胞贴附式和内面向外式膜片钳配置中,当施加20至45 mmHg的吸力时,IKca通道的开放概率增加。低渗肿胀有效地增加了IKca通道电流。当用无钙溶液进行灌流时,低渗肿胀对IKca电流的激活作用减弱。此外,钆(Gd(3+))减弱了低渗肿胀诱导的IKca通道激活,而尼卡地平则没有这种作用。在使用无钙浴液的实验中,用蛋白激酶C(PKC)抑制剂GF109203X预处理可完全消除拉伸诱导的IKca电流激活。细胞松弛素D强烈抑制拉伸诱导的IKca通道激活,表明F-肌动蛋白在通过细胞拉伸变化调节IKca通道中起作用。这些数据表明细胞膜拉伸可激活IKca通道。此外,这种激活与细胞外钙通过拉伸激活的非选择性阳离子通道内流有关,并且还受到F-肌动蛋白细胞骨架和PKC激活的调节。

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