Effect of sodium restriction on urinary excretion of 19-noraldosterone and 18,19-dihydroxycorticosterone, newly identified mineralocorticoids in man.

Abstract

19-Noraldosterone, which was recently shown to be synthesized and produced in the human adrenal gland, possesses potent mineralocorticoid activity. 18,19-Dihydroxycorticosterone [18,19-(OH)2B], a possible precursor of 19-noraldosterone, has also been identified in human urine. To elucidate the regulatory mechanism for these newly described steroids, we studied the effect of sodium restriction on the urinary excretion of 19-noraldosterone and 18,19-(OH)2B in six normal subjects. 18,19-(OH)2B and 19-noraldosterone were measured by specific RIAs after purification of the urine extract by high performance liquid chromatography. The 24-h urinary excretion of 19-noraldosterone and 18,19-(OH)2B during the control period were 107 +/- 40 (+/- SE) pmol/day and 5.6 +/- 0.8 nmol/day, respectively. After sodium restriction, the values increased approximately 2-fold (P less than 0.05), to 259 +/- 76 pmol/day and 15.6 +/- 4.5 nmol/day, respectively. Virtually identical responses were seen for aldosterone (from 21 +/- 6.0 to 38 +/- 10 nmol/day), 18-hydroxycorticosterone (from 9.9 +/- 1.1 to 21 +/- 2.8 nmol/day), and 18-hydroxycortisol (from 377 +/- 93 to 554 +/- 129 nmol/day). These observations suggest that 19-noraldosterone and 18,19-(OH)2B are partly under the control of the renin-angiotensin system in normal subjects.