Effect of norethisterone-acetate on salt excretion and of the renin-aldosterone system in man.
The mechanism of a previously described rise in the excretion rate of aldosterone-18-glucuronide under the influence of norethisterone-acetate was further investigated in 10 male volunteers. Oral administration of 30 mg norethisterone-acetate daily for 1 week caused a significant natriuresis and a rise in the excretion rate of aldosterone-18-glucuronide. Aldosterone secretion rate rose slightly but insignificantly. Plasma aldosterone, renin activity, and angiotensin II remained unaltered while plasma renin substrate increased markedly. Norethisterone-acetate, or one of its metabolites, may directly stimulate aldosterone secretion and metabolism rendering plasma aldosterone levels unaltered. The rise in renin substrate is obviously due to estrogenic properties of the compound studied. The mechanism of natriuresis remains unexplained.
D000328:Adult; D000450:Aldosterone / Q000378:metabolism*; D000804:Angiotensin II / Q000097:blood; D000808:Angiotensinogen / Q000097:blood; D005965:Glucuronates / Q000652:urine; D006801:Humans; D008297:Male; D009640:Norethindrone / Q000031:analogs & derivatives* / Q000494:pharmacology; D012083:Renin / Q000097:blood*; D012964:Sodium / Q000652:urine*
D005965:Glucuronates; D000808:Angiotensinogen; D000804:Angiotensin II; D000450:Aldosterone; D012964:Sodium; D012083:Renin; D009640:Norethindrone