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Ion Channel Regulation by AMPK
Author(s) -
Evans A. Mark,
Hardie D. Grahame,
Peers Chris,
Wyatt Christopher N.,
Viollet Benoit,
Kumar Prem,
Dallas Mark L.,
Ross Fiona,
Ikematsu Naoko,
Jordan Heidi L.,
Barr Barbara L.,
Rafferty J. Nicole,
Ogunbayo Oluseye
Publication year - 2009
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2009.05041.x
Subject(s) - ampk , hypoxic pulmonary vasoconstriction , hypoxia (environmental) , carotid body , amp activated protein kinase , medicine , vasoconstriction , vasodilation , lung , phosphorylation , cardiology , protein kinase a , chemistry , microbiology and biotechnology , biology , carotid arteries , oxygen , organic chemistry
Vital homeostatic mechanisms monitor O 2 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 O 2 deficit to those rich in O 2 , while a fall in arterial pO 2 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 O 2 and thereby energy (ATP) supply at the whole body as well as the cellular level.