Intermittent Hypoxia-Mediated Plasticity of Acute O Sensing Requires Altered Red-Ox Regulation by HIF-1 and HIF-2. Annals of the New York Academy of Sciences [Ann N Y Acad Sci] Journal article

This article provides a brief review of recent studies addressing the effects of chronic intermittent hypoxia (IH) on acute O(2) sensing in carotid bodies (CBs) and adrenal medullary chromaffin cells (AMCs) and the underlying mechanisms. Chronic IH upregulates hypoxic sensing ability of CBs and AMCs in adults and neonates. The effects of IH were reversible in adult rats, whereas that of neonatal IH persist into adult life. Reactive oxygen species (ROS) mediate IH-induced changes in O(2) sensing. Differential regulation of hypoxia-inducible factors 1 and 2 (HIF-1 and 2) contribute to IH-evoked oxidative stress. HIF-1 activation by IH appears to be linked to increased pro-oxidant(s), whereas downregulation of HIF-2 by IH is coupled to transcriptional downregulation of antioxidant enzyme(s). Thus, the studies with chronic IH suggest novel, hitherto uncharacterized, roles for HIF-1 and HIF-2 in regulating red-ox status leading to plasticity of O(2) sensing in CBs and AMCs.

Annals of the New York Academy of Sciences [Ann N Y Acad Sci]