Abundance of Na(+)-K(+)-ATPase mRNA is regulated by glucocorticoid hormones in infant rat kidneys.

The administration of glucocorticoid hormone (GC) accelerates the postnatal maturation of renal Na(+)-K(+)-ATPase activity. This study examines the role of GC for the regulation of the Na(+)-K(+)-ATPase mRNA abundance in renal cortex during development. In 12- to 14-day-old rats an upsurge in serum GC concentration was accompanied by an increase in Na(+)-K(+)-ATPase activity and by an apparent increase in mRNA abundance. In 10-day-old rats injected with a single intraperitoneal dose of betamethasone (T) or diluent (C) the abundances of alpha 1- and beta-mRNAs were 1.8- to 2-fold higher in T than in C rats after 20 min. The mRNA abundance of both subunits was threefold higher after 1 h (P less than 0.01), and it was six- to sevenfold higher after 6 h (P less than 0.01). In any given sample there was a coordinate change in alpha 1- and beta-mRNAs relative to C rats. GC did not appear to induce the expression of any alternative catalytic subunit. The alpha 2-mRNA was not detectable in any experimental protocol. Furthermore, the ouabain inhibition of the Na(+)-K(+)-ATPase, partially purified from the renal cortex, was the same before and after GC. In adult rats injected with betamethasone neither the alpha 1- nor the beta-mRNA abundance was different at any time after injection from those in adult C rats. The rapid onset of the GC effect on mRNA abundance in infant rats suggests that the hormone directly activates the gene for Na(+)-K(+)-ATPase alpha 1-subunit, as well as beta-subunit in the developing kidney, and that GC thereby plays an important role for the postnatal maturation of the kidney.