Key roles for AMP-activated protein kinase in the function of the carotid body?

Christopher N. Wyatt, Selina A. Pearson, Prem Kumar, Chris Peers, D. Grahame Hardie, A. Mark Evans

Research output: Chapter in Book/Report/Conference proceedingConference contribution

Abstract

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.
Original languageEnglish
Title of host publicationIntegration in Respiratory Control
Subtitle of host publicationFrom Genes to Systems
EditorsMarc Poulin, Richard Wilson
PublisherSpringer New York LLC
Pages63-68
Number of pages6
ISBN (Electronic)978-0-387-73693-8
ISBN (Print)978-0-387-73692-1, 978-1-4419-2529-9
DOIs
StatePublished - 2008

Publication series

NameAdvances in Experimental Medicine and Biology
Volume605
ISSN (Print)0065-2598

ASJC Scopus Subject Areas

  • General Biochemistry,Genetics and Molecular Biology

Keywords

  • Carotid Boyd
  • DU145 Cell
  • Intermittent Hypoxia
  • Mitochondrial Oxidative Phosphorylation
  • Chronic Intermittent Hypoxia

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