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氧气诱导小动脉平滑肌细胞中的机电偶联:L型钙通道的作用。

Oxygen induces electromechanical coupling in arteriolar smooth muscle cells: a role for L-type Ca2+ channels.

作者信息

Welsh D G, Jackson W F, Segal S S

机构信息

The John B. Pierce Laboratory and Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut 06519, USA.

出版信息

Am J Physiol. 1998 Jun;274(6):H2018-24. doi: 10.1152/ajpheart.1998.274.6.H2018.

DOI:10.1152/ajpheart.1998.274.6.H2018
PMID:9841528
Abstract

We tested whether O2-induced vasomotor responses of arterioles correspond to changes in membrane potential (Em) of cells in the arteriolar wall. The cheek pouches of anesthetized male hamsters were prepared for intravital microscopy and intracellular recording. Microelectrodes containing Lucifer yellow dye were used to label smooth muscle cells (SMC) or endothelial cells (EC) during arteriolar responses to O2. During low- PO2 superfusion (approximately 20 Torr; arteriolar diameter 55 +/- 2 micron), Em of SMC and EC averaged -37 and -36 mV, respectively. High-PO2 superfusion ( approximately 150 Torr) depolarized SMC (to -15 +/- 1 mV) with vasoconstriction (to 24 +/- 2 micron) and diameter cycled with Em of SMC during vasomotion. In contrast, the Em of EC did not change with PO2 nor during vasomotion, yet Em depolarized by 21 +/- 2 mV when the extracellular K+ concentration ([K+]o) was raised to 55 mM. Superfusion with diltiazem (10 microM) or nifedipine (1 microM) abolished vasomotor and electrical responses to PO2 in SMC but did not eliminate depolarizations to elevated [K+]o. We conclude that, under physiological conditions, electrical and mechanical responses of arteriolar SMC to changes in PO2 are mediated through L-type Ca2+ channels without corresponding electrical activity in EC.

摘要

我们测试了小动脉的氧诱导血管舒缩反应是否与小动脉壁细胞的膜电位(Em)变化相对应。对麻醉的雄性仓鼠的颊囊进行活体显微镜检查和细胞内记录准备。在小动脉对氧的反应过程中,使用含有荧光黄染料的微电极标记平滑肌细胞(SMC)或内皮细胞(EC)。在低氧分压灌注期间(约20托;小动脉直径55±2微米),SMC和EC的Em分别平均为-37和-36毫伏。高氧分压灌注(约150托)使SMC去极化(至-15±1毫伏),伴有血管收缩(至24±2微米),并且在血管运动期间小动脉直径与SMC的Em同步周期性变化。相比之下,EC的Em在氧分压变化时以及血管运动期间均未改变,然而当细胞外钾离子浓度([K+]o)升高至55毫摩尔时,Em去极化21±2毫伏。用硫氮䓬酮(10微摩尔)或硝苯地平(1微摩尔)灌注可消除SMC对氧分压的血管舒缩和电反应,但不能消除对升高的[K+]o的去极化反应。我们得出结论,在生理条件下,小动脉SMC对氧分压变化的电反应和机械反应是通过L型钙通道介导的,而EC中没有相应的电活动。

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