ROLE OF ACTH IN EPISODIC RELEASE OF ALDOSTERONE IN PATIENTS WITH IDIOPATHIC ADRENAL-HYPERPLASIA, HYPERTENSION, AND HYPERALDOSTERONISM

  • 1 January 1976
    • journal article
    • research article
    • Vol. 88  (2) , 261-270
Abstract
The relationship of plasma aldosterone concentration to its identified stimuli was examined in 3 patients with hypertension, hyperaldosteronism and idiopathic adrenal hyperplasia. Four patients with hyperaldosteronism due to adrenal adenomas served as controls. Plasma aldosterone, cortisol, Na and K concentrations and renin activity were measured in blood samples taken at 20 min intervals from 2 a.m. to 8 a.m. during recumbency and sleep. The tests were performed on all patients following a regular Na diet both before and after short-term treatment with dexamethasone. Two of the 3 subjects with adrenal hyperplasia were reexamined after 2 wk of dexamethasone therapy. All 4 control patients with adenomas had episodic increases of plasma aldosterone which were significantly correlated with those of plasma cortisol (r = +0.48 to +0.90). This confirms the previously reported relationship between aldosterone and ACTH in such patients. Two patients with idiopathic adrenal hyperplasia had a similar secretion pattern and a highly significant correlation of the 2 hormones (r = +0.76 and +0.77); one did not (r = +0.13). Short-term dexamethasone pretreatment attenuated the episodic release pattern and partially suppressed the mean plasma concentrations of aldosterone in the 4 patients with an adenoma and in the 2 patients with idiopathic hyperplasia whose plasma aldosterone and cortisol concentrations were positively correlated. There was no such effect in the 3rd patient. The 1st 2 patients with idiopathic hyperplasia were retested following 2 wk of dexamethasone treatment to determine if the episodic secretion pattern of plasma aldosterone would correlate with other stimuli following this period of ACTH suppression. One showed little change from the pattern observed after short-term glucocorticoid treatment. The 2nd had a similarly blunted aldosterone response until ACTH secretion led to a resumption of episodic changes in plasma aldosterone concentrations. ACTH frequently is the dominant stimulus of the episodic secretion of aldosterone in patients with either adrenal adenomas or hyperplasia. When ACTH is suppressed, the hypersecretion of aldosterone is presumably sustained by an intrinsic adrenal abnormality or by an as yet unidentified stimulus.