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Am J Physiol Lung Cell Mol Physiol (September 6, 2002). doi:10.1152/ajplung.00181.2002
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Articles in PresS, published online ahead of print September 6, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00181.2002
Submitted on June 7, 2002
Accepted on September 3, 2002

Hypoxia reversibly inhibits epithelial sodium transport but does not inhibit lung ENaC or Na,K-ATPase expression

Todd C. Carpenter1*, Stacey Schomberg1, Christopher Nichols1, Kurt R. Stenmark1, and John V. Weil2

1 Department of Pediatrics, University of Colorado Health Sciences Center, Denver, CO, USA
2 Cardiovascular-Pulmonary Research Laboratory, University of Colorado Health Sciences Center, Denver, CO, USA

* To whom correspondence should be addressed. E-mail: todd.carpenter{at}uchsc.edu.

Hypoxia reduces alveolar liquid clearance and the nasal potential difference, a marker of airway epithelial sodium transport. The mechanisms underlying this impaired epithelial sodium transport in vivo remain uncertain. We hypothesized that epithelial sodium transport impaired by hypoxia would recover quickly with re-oxygenation, and that hypoxia decreases the expression of lung epithelial sodium channels and Na,K-ATPases. We studied adult rats exposed to normoxia, hypoxia (fiO2 = 0.1) for 24 hours, or hypoxia followed by recovery in normoxia. Nasal potential differences decreased by 40% with hypoxia (p < 0.001), returning to baseline levels with re-oxygenation. Lung Na,K-ATPase activity decreased by 40% with hypoxia (p = 0.003), recovering to baseline levels with re-oxygenation. Lung expression of mRNA encoding for ENaC-{alpha}, -ß, and -{gamma}, or for Na,K-ATPase {alpha}1 did not change significantly with hypoxia or recovery, nor did lung expression of ENaC-{alpha}, ENaC-ß, Na,K-ATPase {alpha}1, or Na,K-ATPase ß1 protein. We conclude that subacute exposure to moderate hypoxia reversibly impairs airway epithelial sodium transport and lung Na,K-ATPase activity, but that those changes are not due to changes in the lung expression of sodium transporting proteins.




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