AJP - Renal Physiology, Vol 260, Issue 2 192-F197, Copyright © 1991 by American Physiological Society
Abundance of Na(+)-K(+)-ATPase mRNA is regulated by glucocorticoid hormones in infant rat kidneys
G. Celsi, A. Nishi, G. Akusjarvi and A. Aperia
Department of Pediatrics, St. Goran's Children's Hospital, Sweden.
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.
