Abstract
Amino-Glutethimide (AG) decreases the secretion rates of aldosterone in control subjects. DOC secretory rate changes are less consistent (with an increase in 3 out of 5) and 18-OH DOC increases evidently in all 5 subjects where measured. Urinary sodium excretion increases after AG. With dexamethasone added to AG to suppress the compensatory increase in ACTH, the DOC and 18-OH DOC secretion rates decrease to the initial levels and further sodium diuresis occurs. Similar changes in urinary sodium excretion occurred in two hypertensive patients, but the blood pressure decreasing effect of AG was not consistent. These results indicate that zonal differences in the response of the adrenal cortex to AG probably exist. The zona glomerulosa, producing aldosterone, is more susceptible to the inhibitory action of AG, while other mineralocorticoids from the zona fasciculata (18-OH DOC and, in part, also DOC) increase as a consequence of the compensatory increase in ACTH. The combination of AG and dexamethasone may prove as a useful tool in suppressing the excessive mineralocorticoid secretion.
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