DEVELOPMENTAL REGULATION OF NA,K-ATPASE IN RAT LUNG

Late in gestation lung epithelium changes from net chloride and fluid secretion to sodium and fluid absorption. Fluid resorption is required for postnatal gas exchange and occurs by combined action of epithelia l sodium channels and Na,K-ATPase. We hypothesized that alveolar epith elial Na,K-ATPase increases perinatally. Immunofluorescence (IF) and i mmunoelectron microscopy (IEM) with a monoclonal anti-alpha subunit an tibody demonstrated that Na,K-ATPase was present on the basolateral su rfaces of columnar epithelial cells at fetal day (FD) 17 and on type I I cells throughout development. However, type I epithelial cells did n ot have detectable Na,K-ATPase. The steady-state levels of both the al isoform and P-subunit mRNAs were maximal at FD20-neonatal day (ND) 1, with consistent increases from the FD 17 level. Na,K-ATPase a-subunit protein also increased from FD17 to FD20-22 and then decreased in the early postnatal period. The ouabain inhibitable sodium pump activity per milligram membrane protein increased 2.6-fold from FD17 to FD22-ND 1 (P < 0.05). The quantities of sodium pump mRNA, antigenic protein, a nd enzyme activity increase in late gestation in accord with a propose d role for Na,K-ATPase in resorption of alveolar sodium and fluid in p reparation for birth.