Chronic stimulation by
adrenocorticotropin (
ACTH) of the adrenal cortex produces different plasma
mineralocorticoid hormone (MCH) patterns, depending on the amount of
glucocorticoid hormones (
cortisol) concurrently generated and the degree of activation of the renin angiotensin system (RAS). Patients with
Cushing's disease or the ectopic
ACTH-excess syndrome have normal or low production of the MCHs,
aldosterone and
18-hydroxycorticosterone (18-OHB), by the zona glomerulosa (ZG), elevated
cortisol and
deoxycorticosterone (DOC) levels, and high-normal to elevated production of the MCHs
corticosterone (B) and
18-hydroxydeoxycorticosterone (18-OHDOC) by the zona fasciculata (ZF). Prolonged administration of superphysiologic doses of
ACTH to normal subjects yields similar patterns. Patients with simple virilizing
21-hydroxylase deficiency (21-OHD) have impaired ZF production of B and 18-OHDOC and elevated DOC, 18-OHB, and
aldosterone secretion secondary to the superimposed RAS stimulation of the ZG. Patients with
17 alpha-hydroxylase deficiency (17 alpha-OHD) have elevated levels of the ZF MCHs DOC, B, 18-OHDOC, and 18-OHB and a functionally suppressed ZG. Patients with
11 beta-hydroxylase deficiency (11 beta-OHD) have only elevated production of DOC by the ZF and suppressed RAS and
aldosterone. A significant negative correlation between
cortisol and
aldosterone concentrations suggests that
cortisol is involved in the
ACTH-mediated inhibition of
aldosterone formation.