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构成肺动脉平滑肌细胞静息电位的钾通道。

Potassium channels underlying the resting potential of pulmonary artery smooth muscle cells.

作者信息

Gurney Alison M, Osipenko Oleg N, MacMillan Debbi, Kempsill Fiona E J

机构信息

Department of Physiology and Pharmacology, Strathclyde Institute for Biomedical Sciences, University of Strathclyde, Glasgow, UK.

出版信息

Clin Exp Pharmacol Physiol. 2002 Apr;29(4):330-3. doi: 10.1046/j.1440-1681.2002.03653.x.

Abstract
  1. The molecular identity of the K channels giving rise to the negative membrane potential of pulmonary artery smooth muscle cells has yet to be determined. 2. To date, most studies have focused on voltage-gated, delayed rectifier channels and their roles in mediating hypoxia-induced membrane depolarization. There is, however, strong evidence that an outwardly rectifying K+ conductance distinct from the classical delayed rectifier is involved. 3. Growing evidence that TASK-like channels can sense hypoxia and are present in pulmonary artery smooth muscle cells suggests that they may be responsible for the resting K+ conductance and resting potential. 4. The present review considers the evidence that particular K channels maintain the resting membrane potential of pulmonary artery smooth muscle cells and mediate the depolarizing response to hypoxia.
摘要
  1. 引起肺动脉平滑肌细胞负膜电位的钾通道的分子特性尚未确定。2. 迄今为止,大多数研究集中在电压门控延迟整流通道及其在介导缺氧诱导的膜去极化中的作用。然而,有强有力的证据表明,存在一种不同于经典延迟整流通道的外向整流钾电导。3. 越来越多的证据表明,类TASK通道能够感知缺氧且存在于肺动脉平滑肌细胞中,这表明它们可能负责静息钾电导和静息电位。4. 本综述探讨了特定钾通道维持肺动脉平滑肌细胞静息膜电位并介导对缺氧的去极化反应的证据。

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