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首页> 外文期刊>American Journal of Physiology >Molecular basis of hypoxia-induced pulmonary vasoconstriction: role of voltage-gated K+ channels.
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Molecular basis of hypoxia-induced pulmonary vasoconstriction: role of voltage-gated K+ channels.

机译：缺氧诱导的肺血管收缩的分子基础：电压门控K +通道的作用。

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摘要

The hypoxia-induced membrane depolarization and subsequent constriction of small resistance pulmonary arteries occurs, in part, via inhibition of vascular smooth muscle cell voltage-gated K+ (KV) channels open at the resting membrane potential. Pulmonary arterial smooth muscle cell KV channel expression, antibody-based dissection of the pulmonary arterial smooth muscle cell K+ current, and the O2 sensitivity of cloned KV channels expressed in heterologous expression systems have all been examined to identify the molecular components of the pulmonary arterial O2-sensitive KV current. Likely components include Kv2.1/Kv9.3 and Kv1.2/Kv1.5 heteromeric channels and the Kv3.1b alpha-subunit. Although the mechanism of KV channel inhibition by hypoxia is unknown, it appears that KV alpha-subunits do not sense O2 directly. Rather, they are most likely inhibited through interaction with an unidentified O2 sensor and/or beta-subunit. This review summarizes the role of KV channels in hypoxic pulmonary vasoconstriction, the recent progress toward the identification of KV channel subunits involved in this response, and the possible mechanisms of KV channel regulation by hypoxia.
机译：缺氧引起的膜去极化和随后的小阻力肺动脉收缩，部分是通过抑制在静息膜电位处开放的血管平滑肌细胞电压门控的K +（KV）通道而发生的。肺动脉平滑肌细胞KV通道表达，基于抗体的肺动脉平滑肌细胞K +电流解剖以及在异源表达系统中表达的克隆KV通道的O2​​敏感性都经过检查，以鉴定肺动脉O2的分子成分敏感的KV电流。可能的组件包括Kv2.1 / Kv9.3和Kv1.2 / Kv1.5异聚通道和Kv3.1bα亚基。尽管尚不清楚缺氧抑制KV通道的机制，但似乎KVα亚基不能直接感应O2。相反，它们最有可能通过与未知O2传感器和/或β-亚基的相互作用而被抑制。这篇综述总结了KV通道在缺氧性肺血管收缩中的作用，最近对鉴定参与该反应的KV通道亚单位的进展以及缺氧调节KV通道的可能机制。

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