AMP-Activated Protein Kinase and Chemotransduction in the Carotid Body
Document Type
Article
Publication Date
7-2007
Abstract
AMP-activated protein kinase (AMPK) is a key component of a kinase cascade that regulates energy balance at the cellular level. Our recent research has raised the possibility that AMPK may also function to couple hypoxic inhibition of mitochondrial oxidative phosphorylation to O2-sensitive K+ channel inhibition and hence underpin carotid body type I cell excitation. Thus, in addition to maintaining the cellular energy state AMPK may act as the primary metabolic sensor and effector of hypoxic chemotransduction in type I cells. These findings provide a unifying link between two previously separate theories pertaining to O2-sensing in the carotid body, namely the ‘membrane hypothesis’ and the ‘mitochondrial hypothesis’. Furthermore, our data suggest that in addition to its effects at the cellular level the AMPK signalling cascade can mediate vital physiological mechanisms essential for meeting the metabolic needs of the whole organism.
Repository Citation
Wyatt, C. N.,
& Evans, A. M.
(2007). AMP-Activated Protein Kinase and Chemotransduction in the Carotid Body. Respiratory Physiology & Neurobiology, 157 (1), 22-29.
https://corescholar.libraries.wright.edu/ncbp/205
DOI
10.1016/j.resp.2007.01.021