Journal
RESPIRATORY PHYSIOLOGY & NEUROBIOLOGY
Volume 174, Issue 3, Pages 230-234Publisher
ELSEVIER
DOI: 10.1016/j.resp.2010.08.022
Keywords
NADPH oxidases; Mitochondrial electron transport chain; S-glutathionylation; T-type Ca2+ channels; Ryanodine receptors; Endothelin; 5-HT
Categories
Funding
- National Institutes of Health, Heart, Lung and Blood Institute [HL-90554, HL-76537, HL-86493, HL-089616]
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Carotid bodies and neonatal adrenal medullary chromaffin cells (AMC) respond rapidly to acute hypoxia before compromising cellular functions. Responses to acute hypoxia are dynamically altered by chronic perturbations in arterial blood O-2 levels resulting from breathing disorders. Sleep disordered breathing with recurrent apneas cause periodic decreases in arterial blood O-2 or intermittent hypoxia (IH). Recent studies suggest that reactive oxygen species (ROS) mediate cellular adaptations to prolonged hypoxia. In this article we discuss the evidence for ROS in mediating exaggerated carotid body and AMC responses to acute hypoxia by IH and the underlying cellular and molecular mechanisms. IH increases ROS levels, and anti-oxidants prevent IH-induced augmented responses of the carotid body and AMC to hypoxia. The enhanced hypoxic sensitivity by IH involves ROS-dependent recruitment of transmitters/modulators in the carotid body and Ca2+ signaling mechanisms in AMC. Mechanisms by which IH elevates ROS include activation of NADPH oxidases, inhibition of mitochondrial complex I activity and down-regulation of anti-oxidant enzymes. Transcriptional regulation of pro- and anti-oxidant enzymes by hypoxia-inducible factors 1 and 2 appears to be a major molecular mechanism regulating ROS generation by IH. (C) 2010 Elsevier B.V. All rights reserved.
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