Suppression of aldosterone biosynthesis by treatment of rats with adrenocorticotropin: comparison with glucocorticoid effects.
The treatment of rats with a high dose of ACTH resulted within 4 days in a marked suppression of aldosterone and deoxycorticosterone outputs by capsular adrenal tissue ("zona glomerulosa") incubated with and without serotonin and in decreased conversions of tritiated corticosterone and deoxycorticosterone to aldosterone and 18-hydroxycorticosterone, but in strikingly increased capsular adrenal conversions of tritiated deoxycorticosterone to corticosterone and 18-hydroxy deoxycorticosterone. ACTH also suppressed aldosterone biosynthesis in rats kept on a sodium-deficient diet. Corticosterone or dexamethasone, when added to the drinking fluid for 2 weeks, induced only small decreases in aldosterone biosynthesis from endogenous or exogenous precursors. Moreover, they significantly decreased the capsular adrenal conversion of added deoxycorticosterone to corticosterone and 18-hydroxydeoxycorticosterone. These results indicate that during prolonged ACTH treatment, the zona glomerulosa cell may be converted to a functional zona fasciculata type of cell. High levels of circulating mineralocorticoids and glucocorticoids seem to be minor contributory factors in the long term suppression of aldosterone biosynthesis by ACTH.
D000311:Adrenal Glands / Q000033:anatomy & histology / Q000187:drug effects / Q000378:metabolism*; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology*; D000450:Aldosterone / Q000096:biosynthesis*; D000818:Animals; D003345:Corticosterone / Q000494:pharmacology*; D003900:Desoxycorticosterone / Q000096:biosynthesis*; D003907:Dexamethasone / Q000494:pharmacology*; D008297:Male; D009929:Organ Size; D011188:Potassium / Q000097:blood; D051381:Rats; D012964:Sodium / Q000097:blood
D003900:Desoxycorticosterone; D000450:Aldosterone; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone; D012964:Sodium; D011188:Potassium; D003345:Corticosterone