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1 Department of Pediatrics (Section of Respiratory Medicine), Yale University School of Medicine, New Haven, CT, USA; Department of Pediatrics (Section of Respiratory Medicine), Albert Einstein College of Medicine, Bronx, NY, USA
2 Department of Pediatrics (Section of Respiratory Medicine), Yale University School of Medicine, New Haven, CT, USA
3 Molecular Medicine and Renal Units, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA
4 Department of Pediatrics (Section of Respiratory Medicine), Yale University School of Medicine, New Haven, CT, USA; Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT, USA; Department of Pediatrics (Section of Respiratory Medicine), Albert Einstein College of Medicine, Bronx, NY, USA
* To whom correspondence should be addressed. E-mail: ghaddad{at}aecom.yu.edu.
Chronic intermittent hypoxia (CIH) is a component of several disease states including obstructive sleep apnea which results in neurocognitive and cardiovascular morbidity. Since chronic hypoxia can induce changes in metabolism and pH homeostasis, we hypothesized that CIH induces changes in the expression of acid-base transporters. P02-03 mice, exposed to alternating cycles of 2 min of hypoxia (6.0-7.5% O2) and 3 min of normoxia (21% O2) for 8h per day for 28d, demonstrated decreases in specific acid-base transport protein expression in most of the CNS. NHE-1 and NBC expression was decreased in all regions of the CNS but especially so in the cerebellum. NHE-3, which is only expressed in the cerebellum, was also significantly decreased. AE-3 protein was decreased in most brain regions, with the decrease being substantial in the hippocampus. These results indicate that CIH induces down-regulation of the major acid-extruding transport proteins, NHE1 and NBC, in particular regions of the CNS. This down-regulation in acid-extruding capacity may render neurons more prone to acidity and possibly to injury during CIH, especially in cerebellum and hippocampus. Alternatively, it is possible that O2 consumption in these regions is decreased after CIH with consequential down-regulation in the expression of certain cellular proteins that may be less needed under such circumstances.
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