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Copyright ©ERS Journals Ltd 2001
Molecular physiology of oxygen-sensitive potassium channels
Institut de Pharmacologie Moléculaire et Cellulaire, Valbonne, France
CORRESPONDENCE: E. Honoré, Institut de Pharmacologie Moléculaire et Cellulaire, CNRS - UMR6097, 660 route des Lucioles, Sophia Autipolis,, 06560, Valbonne, France. Fax: 33 493957704
Keywords: Acute hypoxia, neutroepithelial body cells, oxygen sensors, potassium channel
Received: January 9, 2001
Accepted March 7, 2001
This work was supported by the Centre National de la Recherche Scientifique (CNRS).
Abstract
Physiological adaptation to acute hypoxia involves oxygen-sensing by a variety of specialized cells including carotid body type I cells, pulmonary neuroepithelial body cells, pulmonary artery myocytes and foetal adrenomedullary chromaffin cells.
Hypoxia induces depolarization by closing a specific set of potassium channels and triggers cellular responses. Molecular biology strategies have recently allowed the identification of the K+ channel subunits expressed in these specialized cells.
Several voltage-gated K+ channel subunits comprising six transmembrane segments and a single pore domain (Kv1.2, Kv1.5, Kv2.1, Kv3.1, Kv3.3, Kv4.2 and Kv9.3) are reversibly blocked by hypoxia when expressed in heterologous expression systems. Additionally, the background K+ channel subunit TASK-1, which comprises four transmembrane segments and two pore domains, is also involved in both oxygen- and acid-sensing in peripheral chemoreceptors.
Progress is currently being made to identify the oxygen sensors. Regulatory ß subunits may play an important role in the modulation of Kv channel subunits by oxygen.
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