Expression of the α-subunit of Na/K-ATPase in renal collecting duct epithelium during development

Minuth, Will W.; Gross, Peter; Gilbert, Peter; Kashgarian, Michael
May 1987
Kidney International;May1987, Vol. 31 Issue 5, p1104
Academic Journal
Aldosterone enhances synthesis and enzyme activity of Na/K-ATPase and has been found to stimulate sodium reabsorption by the renal cortical collecting duct. Moreover, chrome exposure to aldosterone is associated with a remarkable morphological-functional adaptation. This is seen as a magnification in basolateral membrane area of principal cells. In the present paper we investigated the acquisition of Na/K-ATPase α-subunit in renal tissue and examined whether aldosterone initiates functional and adaptive changes in cultured collecting duct cells similar to those observed in vivo. Using a monoclonal antibody, immunofluorescence microscopy demonstrated the acquisition of the a-subunit of Na/K-ATPase m the developing cortical collecting ducts of the kidney of neonatal rabbits. The mature collecting ducts in the medulla and papilla of the developing kidney were strongly labelled at the basolateral side, while in the cortical portion of the fetal collecting duct adjacent to the embryonic ampullae the immunolabel was found at the apical and the basolateral aspect of the epithelium. However, the embryonic collecting duct ampullae in the outer cortex did not show any reaction with the antibody. In the collecting duct cells cultured for 24 hours the α-subunit of Na/K-ATPase was found to be distributed at both the apical and basolateral aspect of the epithelium. After two to 16 days, the immunolabel was strictly found distributed at the basolateral side. Culturing collecting duct cells in the presence of aldosterone (10-6 M), the hormone modulated the cellular shape of epithelia after five days by infolding the lateral plasma membranes. Simultaneously cellular height of aldosterone treated cells was approximately 25% less than in controls indicating a ‘shrinkage’ of the cells consequent to infolding of excessive lateral plasma membrane.


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