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1 & 2 subunits of the Na,K-ATPase reduces maximal alveolar epithelial fluid clearance
1 Cardiovascular Research Institute and the Departments of Medicine and Anesthesia, University of California, San Francisco, San Francisco, CA, USA
2 Department of Zoology, Miami University, Oxford, OH, USA
3 Department of Molecular Genetics, University of Cincinnati, Cincinnati, OH, USA
* To whom correspondence should be addressed. E-mail: mlooney{at}itsa.ucsf.edu.
Impaired ENaC function predisposes to delayed resorption of pulmonary edema and more severe experimental lung injury, whereas even a small fraction of the normal Na,K-ATPase activity is thought to be sufficient to maintain normal ion transport. However, direct proof is lacking. Therefore, we studied baseline and cAMP stimulated alveolar fluid clearance (AFC) in mice with a 50% decrease in lung protein expression of the 
1 and/or 2 subunit of the Na,K-ATPase. There was no difference in basal and stimulated AFC in 1+/- or 2+/- mice compared to wild type littermates. Also, the compound heterozygous mice (1+/-/2+/-) had normal basal AFC. However, the combined 1+/-/2+/- mice showed a significant decrease in cAMP stimulated AFC compared to wild type littermates (11.1 ± 1.0 vs. 14.9 ± 1.8 %/30 min, P<0.001). When exposed to 96 h of > 95% hyperoxia, the decrease in stimulated AFC in the 1+/-/2+/- mice was not associated with more lung edema compared to wild type littermates (lung wet-to-dry weight ratio 6.6 ± 0.9 vs. 5.9 ± 1.1, respectively, P=NS). Thus, a 50% decrease in protein expression of the 1 or 2 subunits of the Na,K-ATPase does not impair basal or stimulated AFC. However, a 50% protein reduction in both the 1 and 2 subunits of the Na,K-ATPase produces a sub-maximal stimulated AFC, suggesting a synergistic role for 1 and 2 subunits in cAMP dependent alveolar epithelial fluid clearance.
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