RT Journal Article
SR Electronic
T1 Molecular physiology of oxygen-sensitive potassium channels
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP 221
OP 227
DO 10.1183/09031936.01.00204001
VO 18
IS 1
A1 A.J. Patel
A1 E. Honoré
YR 2001
UL http://erj.ersjournals.com/content/18/1/221.abstract
AB 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 β subunits may play an important role in the modulation of Kv channel subunits by oxygen.This work was supported by the Centre National de la Recherche Scientifique (CNRS).