THE EFFECT OF AMILORIDE AND SODIUM-CHLORIDE ON RAT RENAL AND HEPATIC 11-BETA-HYDROXYSTEROID DEHYDROGENASE-ACTIVITIES

The ability of glucocorticoid hormones to interact with glucocorticoid or mineralocorticoid receptors is modulated by 11 beta-hydroxysteroid dehydrogenases, interconverting active 11 beta-hydroxyglucocorticoids to inactive 11-ketones. This is, amongst others, important in maintai ning a normal salt-water homeostasis. In this study, we determined the effect of treating rats for 4 days with the potassium sparing diureti c amiloride (5 mg/kg subcutaneously) or with 3% NaCl in drinking water on renal and hepatic microsomal oxidative and reductive 11 beta-hydro xysteroid dehydrogenase activities and immunoreactive 11 beta-hydroxys teroid dehydrogenase 1 protein. Treatment with amiloride resulted in a 1.5-fold rise of microsomal corticosterone 11 beta-oxidation rates in kidney (using NAD and NADP as cofactors) and in liver (for NADP only) , but had no effect on microsomal 11-dehydrocorticosterone reduction. Renal 11 beta-hydroxysteroid dehydrogenase 1 immunoreactive protein wa s increased 1.6-fold by amiloride. NaCl treatment appeared to have no effect.