Molecular physiology of oxygen-sensitive potassium channels.
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 beta subunits may play an important role in the modulation of Kv channel subunits by oxygen.[1]References
- Molecular physiology of oxygen-sensitive potassium channels. Patel, A.J., Honoré, E. Eur. Respir. J. (2001) [Pubmed]
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