Quartered adrenal glands of rats kept on a sodium-deficient diet or uremic after bilateral nephrectomy were found to produce more aldosterone and less deoxycorticosterone in vitro than adrenal tissue of normal rats. On the other hand, dietary potassium deficiency led to a decreased aldosterone production and an increased deoxycorticosterone production. These differences in corticosteroid production became especially marked when the adrenals were stimulated in vitro by serotonin, adrenocorticotropin (ACTH) or a high potassium concentration in the incubation medium. In adrenals of sodium-deficient or uremic rats aldosterone production was stimulated to the same extent by the addition of progesterone, deoxycorticosterone or corticosterone, whereas in normal adrenal tissue aldosterone production was highest when corticosterone was added to the incubation medium. Only added corticosterone significantly stimulated aldosterone production in adrenals of potassium-deficient rats. These results indicate that the steroidogenic response of adrenal tissue to serotonin, potassium ions and ACTH was dependent on enzyme activities at 2 different levels of aldosterone biosynthesis, i.e., 11β-hydroxylation and one or both of the reactions involved in the conversion of corticosterone to aldosterone. These steps were activated by sodium deficiency and uremia, and inactivated by potassium deficiency. The width of the zona glomerulosa of the adrenal cortex was found to be distinctly increased in sodium-deficient rats, moderately decreased in potassium-deficient rats, but normal in uremic rats. Thus, the marked alterations of the steroidogenic response observed in this last group of animals were independent of morphological changes of the adrenal cortex. (Endocrinology85: 43, 1969)
No takes yet. Share an insight, caveat, or question.
Müller et al. (1969) studied this question.