Yusufi A N, Moltaji H, Dousa T P
Nephrology Research Unit, Mayo Clinic and Foundation Rochester, MN 55905.
Biochem Biophys Res Commun. 1989 Jun 30;161(3):1160-5. doi: 10.1016/0006-291x(89)91363-6.
Dexamethasone administered to rats blocks and/or reverses adaptive increases in the rate of Na+-Pi cotransport, and also in the Na+-dependent binding of [14C]-phosphonoformic acid (PFA) by renal brush border membrane (BBM) vesicles elicited by thyroid hormone (T3). In contrast, dexamethasone had no effect on Na+-independent binding of [14C]-phosphonoformic acid, on Na+-dependent transport of D-glucose or on Na+-dependent binding of phlorizin by BBMV which indicates that its inhibitory effect is specific for Na+-Pi cotransport system of BBM. These findings suggest that glucocorticoids antagonize T3-elicited adaptive enhancement of Na+-Pi cotransport in renal proximal tubules by blocking the T3-stimulated de novo synthesis of Na+-Pi symporters and/or their insertion into BBM.
