The carotid bodies play a critical role in initiating compensatory ventilatory responses to hypoxia. However, the complete mechanism by which hypoxia excites the oxygen-sensing carotid body type 1 cells has not been fully defined. We have previously proposed that the enzyme adenosine monophosphateactivated protein kinase (AMPK) may couple hypoxic inhibition of mitochondrial oxidative phosphorylation to carotid body type I cell excitation (Evans, Mustard, Wyatt, Peers, Dipp, Kumar, Kinnear and Hardie 2005). Here we discuss evidence that AMPK is a key requirement for hypoxic chemotransduction by the carotid body. In addition, we postulate upon a role for AMPK in the plasticity observed in the carotid body during both chronic and chronic intermittent hypoxia. © 2008 Springer Science+Business Media, LLC.
CITATION STYLE
Wyatt, C. N., Pearson, S. A., Kumar, P., Peers, C., Hardie, D. G., & Evans, A. M. (2008). Key roles for AMP-activated protein kinase in the function of the carotid body? In Advances in Experimental Medicine and Biology (Vol. 605, pp. 63–68). https://doi.org/10.1007/978-0-387-73693-8_11
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