Differential effects of glucocorticoids and mineralocorticoids on the mRNA expression of colon ion transporters in infant rats

Several epithelial ion transporters are developmentally regulated in the preweaning period, at the time when the circulating levels of glucocorticoid and mineralocorticoid hormones increase. The specific role of glucocorticoids and mineralocorticoids in the maturation of epithelial ion transport is still disputed. In this study, we investigated the effect of corticosteroids on the mRNA expression of ion transporters in the infant rat colon, a glucocorticoid- and mineralocorticoid-sensitive organ. The expression of the Na, K-ATPase, the H, K-ATPase and the amiloride-sensitive Na⁺ channel mRNA was investigated in control rats from fetal to adult life. We found that the mRNA of the three transporters is temporarily up-regulated in the preweaning period. Rats were then injected with a single dose of betamethasone or aldosterone at 10 d of age. The main effect was the glucocorticoid stimulation of the Na, K-ATPase mRNA within 6 h (4-fold). Glucocorticoids did not alter H, K-ATPase nor Na⁺ channel mRNA within 6 h. Aldosterone moderately (1.7-fold) stimulated Na⁺ channel within 6 h, but did not alter Na, K-ATPase nor H, K-ATPase mRNA. Twenty-four hours after injection, both glucocorticoids and mineralocorticoids had less pronounced and distinct effects. In tissue with lower aldosterone receptor abundance (renal cortex) or with no aldosterone receptor (stomach), glucocorticoids induce a similarly rapid increases in Na, K-ATPase mRNA (4-fold within 6 h), whereas aldosterone had no effect within 6 h. However, glucocorticoids did not stimulate Na, K-ATPase mRNA in the brain, a tissue rich in glucocorticoid receptors. This study indicates that Na, K-ATPase is a primary target for glucocorticoids in the preweaning period, and suggests that glucocorticoid induction of Na, K-ATPase mRNA may play an important role in the maturation of epithelial ion transport capacity. The effect is probably mediated by glucocorticoids and not by mineralocorticoid receptors. However, it seems that an auxiliary factor is required for glucocorticoid-dependent stimulation of Na, K-ATPase mRNA.