Kv2.1/Kv9.3, a novel ATP-dependent delayed-rectifier K+ channel in oxygen-sensitive pulmonary artery myocytes

被引：243

作者：

Patel, AJ ^{[1
]}

Lazdunski, M ^{[1
]}

Honore, E ^{[1
]}

机构：

[1] CNRS,INST PHARMACOL MOL & CELLULAIRE,F-06560 VALBONNE,FRANCE

来源：

EMBO JOURNAL | 1997年 / 16卷 / 22期

关键词：

dex-fenfluramine; hypoxia; oxygen-sensitivity; pulmonary hypertension; vasoconstriction;

D O I：

10.1093/emboj/16.22.6615

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The molecular structure of oxygen-sensitive delayed-rectifier K+ channels which are involved in hypoxic pulmonary artery (PA) vasoconstriction has yet to be elucidated. To address this problem, we identified the Shab K+ channel Kv2.1 and a novel Shab-like subunit Kv9.3, in rat PA myocytes, Kv9.3 encodes an electrically silent subunit which associates with Kv2.1 and modulates its biophysical properties, The Kv2.1/9.3 heteromultimer, unlike Kv2.1, opens in the voltage range of the resting membrane potential of PA myocytes, Moreover, we demonstrate that the activity of Kv2.1/Kv9.3 is tightly controlled by internal ATP and is reversibly inhibited by hypoxia, In conclusion, we propose that metabolic regulation of the Kv2.1/Kv9.3 heteromultimer may play an important role in hypoxic PA vasoconstriction and in the possible development of PA hypertension.

引用

页码：6615 / 6625

页数：11