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Article
Ion Channel Regulation by AMPK: The Route of Hypoxia-Response Coupling in the Carotid Body and Pulmonary Artery
Annals of the New York Academy of Sciences
  • A. Mark Evans
  • D. Grahame Hardie
  • Chris Peers
  • Christopher N. Wyatt, Wright State University - Main Campus
  • Benoit Viollet
  • Prem Kumar
  • Mark L. Dallas
  • Fiona A. Ross
  • Naoko Ikematsu
  • Heidi L. Jordan
  • Barbara L. Barr, Wright State University - Main Campus
  • J. Nicole Rafferty
  • Oluseye Ogunbayo
Document Type
Article
Publication Date
10-1-2009
Abstract
Vital homeostatic mechanisms monitor O2 supply and adjust respiratory and circulatory function to meet demand. The pulmonary arteries and carotid bodies are key systems in this respect. Hypoxic pulmonary vasoconstriction (HPV) aids ventilation−perfusion matching in the lung by diverting blood flow from areas with an O2 deficit to those rich in O2, while a fall in arterial pO2 increases sensory afferent discharge from the carotid body to elicit corrective changes in breathing patterns. We discuss here the new concept that hypoxia, by inhibiting oxidative phosphorylation, activates AMP-activated protein kinase (AMPK) leading to consequent phosphorylation of target proteins, such as ion channels, which initiate pulmonary artery constriction and carotid body activation. Consistent with this view, AMPK knockout mice exhibit an impaired ventilatory response to hypoxia. Thus, AMPK may be sufficient and necessary for hypoxia-response coupling and may regulate O2 and thereby energy (ATP) supply at the whole body as well as the cellular level.
DOI
10.1111/j.1749-6632.2009.05041.x
Citation Information
A. Mark Evans, D. Grahame Hardie, Chris Peers, Christopher N. Wyatt, et al.. "Ion Channel Regulation by AMPK: The Route of Hypoxia-Response Coupling in the Carotid Body and Pulmonary Artery" Annals of the New York Academy of Sciences Vol. 1177 Iss. 1 (2009) p. 89 - 100 ISSN: 1749-6632
Available at: http://works.bepress.com/christopher_wyatt/40/