Premium
Intermittent Hypoxia‐Mediated Plasticity of Acute O 2 Sensing Requires Altered Red‐Ox Regulation by HIF‐1 and HIF‐2
Author(s) -
Prabhakar Nanduri R.,
Kumar Ganesh K.,
Nanduri Jayasri
Publication year - 2009
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2009.05034.x
Subject(s) - downregulation and upregulation , hypoxia (environmental) , intermittent hypoxia , oxidative stress , reactive oxygen species , carotid body , microbiology and biotechnology , chemistry , endocrinology , oxygen , medicine , biology , gene , biochemistry , electrophysiology , organic chemistry , obstructive sleep apnea
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.