Glucocorticoids differentially regulate the mRNA for Na+, K+-ATPase isoforms in infant rat heart

Abstract

The postnatal maturation of Na+, K+-ATP-ase a- and /3-subunit genes can be accelerated in the rat kidney by the administration of glucocorticoid hormones (GC). In heart, Na+, K+-ATPase a-isoform and /J-subunit genes exhibit a complex pattern of expression during development. This study examines the role of GC in the regulation of Na+, K+-ATPase mRNA abundance in rat heart during infancy. In 10-d-old rats given injections with a single intraperitoneal dose of betamethasone or diluent, the Na+, K+-ATPase activity was 2-fold higher in treated than in control rats after 24 h. GC differentially regulated the mRNA for Na+, K+-ATPase subunits. A significant increase in Na+, K+-ATPase mRNA occurred with a dose of 2.5 ng betamethasone/100 g body weight. The following experiments were performed with a saturating dose of 60 jtg betamethasone/100 g body weight. The al mRNA was moderately but significantly increased (1.5-fold) 6 h after treatment. The mRNA for the al subunit increased 2.2-fold after betamethasone treatment. The mRNA for β1 was numerically increased after 20 min (1.3-fold); it was 1.5-fold higher (p < 0.05) after 1 h and was 3-fold higher after 6 h (p < 0.01). Betamethasone treatment did not significantly change the abundance of the mRNA for the «3 subunit. The expression of actin mRNA was not altered after GC. These data indicate that GC hormones may act as a “molecular switch” in the developmental expression of the mRNA for the Na+, K+-ATPase a-isoforms and contribute in stimulating the maturation of rat heart during the preweaning period. © 1992 International Pediatric Research Foundation, Inc.