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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.

Pubmed ID: 9362476


  • Patel AJ
  • Lazdunski M
  • HonorĂ© E


The EMBO journal

Publication Data

November 17, 1997

Associated Grants


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