Regulation of Aldosterone Biosynthesis During Sodium Deficiency

The aldosterone response to adreoocorticotropic hormone (ACTH) and angiotensin II (AH) was evaluated in patients with pituitary insufficiency before and after dietary sodium restriction (10 mEq Na+/day for 12 days). On normal sodium intake, plasma aldosterone concentration and plasma cortisol concentration failed to change from control levels in response to a single injection of ACTH or to a continuous 1hour infusion of AH in patients with pituitary insufficiency. In response to dietary sodium restriction for 12 days, plasma renln activity (PRA) increased fivefold in patients with pituitary insufficiency, while plasma aldosterone concentration failed to increase significantly, averaging 11.0 ± 3.1 before and 123 ± 3.7 ng/dl (ns, p > 0.05) after sodium deficiency. Although aldosterone secretion failed to increase during sodium deficiency, the patients came into balance at 10 mEq without a significant change in arterial blood pressure (BP). In sharp contrast to the lack of aldosterone response to ACTH before sodium deficiency, plasma aldosterone concentration increased markedly from 12.9 ± 3 J to 156 ± 17.3 ng/dl (p < 0.001) in response to ACTH after sodium deficiency. Although the adrenal glomerulosa cells were markedly sensitive to ACTH during sodium deficiency, they remained almost totally refractory to AH since aldosterone secretion failed to increase significantly in response to continuous infusion of a pressor dose of All for 1 hour. Replacement therapy with ACTH gel for 3 months in patients with pituitary insufficiency failed to restore a normal aldosterone response to either ACTH or AH. These data demonstrate that some non-ACTH pituitary factors) is essential for a normal aldosterone response to ACTH, AH, and sodium deficiency. (Hypertension 3 (supp I): I-74-I-80, 1981)