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 maintaining a normal salt-water homeostasis. In this study, we determined the effect of treating rats for 4 days with the potassium sparing diuretic amiloride (5 mg/kg subcutaneously) or with 3% NaCl in drinking water on renal and hepatic microsomal oxidative and reductive 11 beta-hydroxysteroid dehydrogenase activities and immunoreactive 11 beta-hydroxysteroid 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 was increased 1.6-fold by amiloride. NaCl treatment appeared to have no effect.