Kv2.1/Kv9.3, a novel ATP-dependent delayed-rectifier K+ channel in oxygen-sensitive pulmonary artery myocytes
Kv2.1/Kv9.3, a novel ATP-dependent delayed-rectifier K+ channel in oxygen-sensitive pulmonary artery myocytes
复制标题
DOI：
10.1093/emboj/16.22.6615
复制
发表时间：
1997-11-17
期刊：
影响因子：
11.4
通讯作者：
Honore, E
中科院分区：
文献类型：
--
作者：
Patel, AJ;Lazdunski, M;Honore, E
氧敏感延迟整流钾通道参与缺氧性肺动脉(PA)血管收缩，其分子结构尚不清楚。为了解决这个问题，我们在大鼠PA心肌细胞中发现了一个新的Shab K+通道Kv2.1和一个新的类Shab亚基Kv9.3，Kv9.3编码一个与Kv2.1相关的电子沉默亚基，并调节其生物物理特性。与Kv2.1不同，Kv2.1/9.3异多聚体开放在PA肌细胞静息膜电位的电压范围内，此外，我们证明Kv2.1/Kv9.3的活性受到内部ATP的严格控制，并可被低氧抑制。我们认为Kv2.1/Kv9.3异多聚体的代谢调节可能在缺氧性PA血管收缩和PA高血压的可能发展中起重要作用。
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.