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

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.
Mesh Terms:
Adenosine Triphosphate, Amino Acid Sequence, Anaerobiosis, Animals, Cloning, Molecular, Delayed Rectifier Potassium Channels, Ion Channel Gating, Molecular Sequence Data, Muscle, Smooth, Vascular, Oxygen, Phylogeny, Potassium Channels, Potassium Channels, Voltage-Gated, Protein Binding, Pulmonary Artery, Rats, Rats, Sprague-Dawley, Recombinant Proteins, Sequence Analysis, DNA, Sequence Homology, Amino Acid, Shab Potassium Channels
EMBO J.
Date: Nov. 17, 1997
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