11β-Hydroxylation of 18-hydroxy-11-deoxycorticosterone by rat adrenal tissue: Zone specificity and effect of sodium and potassium restriction

Abstract

The 11β-hydroxylation of substrate amounts of tritiated 18-hydroxy-11-deoxycorticosterone (18-OH-DOC) by incubated separate zones of the rat adrenal cortex was measured and compared with the 11β-hydroxylation of deoxycorticosterone and 11-deoxycortisol and with the conversion of corticosterone to 18-hydroxycorticosterone. In capsular adrenal tissue (“zona glomerulosa”), 18-OH-DOC, deoxycorticosterone and 11-deoxycortisol were converted to 11β-hydroxysteroids to a similar extent. In the decapsulated portions of the adrenal cortex, the 11β-hydroxylation of 18-OH-DOC was substantially lower than the 11β-hydroxylation of the other two steroids. In both portions of the adrenal cortex more 18-hydroxycorticosterone was produced from added 18-OH-DOC than from added corticosterone. An increased conversion of 18-OH-DOC to 18-hydroxycorticosterone by capsular adrenals of sodiumdeficient rats was observed, but only when the precursor steroid was added at a very high concentration. At all substrate concentrations tested, significantly less 18-OH-DOC was converted to its 11β-hydroxy derivative by capsular adrenals of potassium-deficient rats than by tissue of potassium-replete animals. These findings indicate that the 11β-hydroxylation of 18-OH-DOC is a reaction characteristic of the zona glomerulosa and is regulated in response to alterations in the body sodium and potassium status.