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Kv2.1/Kv9.3, a novel ATP‐dependent delayed‐rectifier K + channel in oxygen‐sensitive pulmonary artery myocytes
Author(s) -
Patel Amanda J.,
Lazdunski Michel,
Honoré Eric
Publication year - 1997
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/16.22.6615
Subject(s) - biology , myocyte , inward rectifier potassium ion channel , oxygen , potassium channel , pulmonary artery , medicine , biophysics , cardiology , microbiology and biotechnology , anatomy , biochemistry , ion channel , receptor , physics , quantum mechanics
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.