The conversion of 18-hydroxycorticosterone and 18-hydroxy-11-deoxycorticosterone to aldosterone by rat adrenal tissue: Evidence for an alternative biosynthetic pathway

Abstract

Substrate amounts of tritiated deoxycorticosterone, corticosterone, 18-hydroxy-11-deoxycorticosterone (18-OH-DOC) and 18-hydroxycorticosterone were incubated with capsular portions of rat adrenal glands (“zona glomerulosa”), and the conversions of these steroids to aldosterone were measured. Tissue from normally fed, sodium-restricted and potassium-restricted animals was used. The main findings were: 1. At low precursor concentrations, corticosterone and deoxycorticosterone were converted to aldosterone 9–25 times more efficiently than their respective 18-hydroxy derivatives. At higher concentrations, the relative convertibility of the 18-hydroxy steroids increased.2. At low precursor concentrations, significantly more deoxycorticosterone than corticosterone was converted to aldosterone. At higher concentrations, corticosterone was converted to aldosterone at least as efficiently as deoxycorticosterone. 3. Twice as much 18-OH-DOC as 18-hydroxycorticosterone was converted to aldosterone, irrespective of the precursor concentration. 4. All four conversions equally increased and decreased in response to sodium restriction and potassium restriction, respectively. These results indicate that up to 50% of the aldosterone derived from deoxycorticosterone may be formed by a pathway including 18-OH-DOC instead of corticosterone. In addition, the activity of the enzyme system responsible for the conversion of 18-hydroxycorticosterone to aldosterone appears to be regulated in response to alterations in the body sodium or potassium status.