Role of Growth Hormone in the Regulation of Aldosterone Biosynthesis*

Experimental evidence indicates that a non-ACTH pituitary hormone (s) is essential for a normal aldosterone response to ACTH and sodium deprivation in man and animals. The present study was designed to evaluate the role of somatotropin in the regulation of aldosterone biosynthesis in human beings. The aldosterone response to ACTH was determined in 8 intact human beings before and after dietary sodium restriction and compared with the aldosterone response observed in 3 patients with panhypopituitarism and 3 patients with isolated GH deficiency. Plasma aldosterone concentration, plasma cortisol concentration, and plasma renin activity were determined by radioimmunoassay. A normal aldosterone,cortisol, and renin response to dietary sodium restriction and ACTH was observed in the subjects with isolated GH deficiency. Plasma aldosterone concentration was normal under resting conditions in the patients with panhypopituitarism, but failed to increase in response to ACTH or sodium deprivation. A normal response of plasma renin activity to sodium deprivation was observed in the subjects with panhypopituitarism. A marked increase in the sensitivity of the adrenal glomerulosa to ACTH was observed in normal subjects and in subjects with isolated GH deficiency and panhypopituitarism during sodium deficiency. The subjects with isolated GH deficiency and panhypopituitarism were maintained on hGH replacement therapy for 12 months. All 6 subjects showed an increased growth rate, but GH replacement therapy failed to restore a normal aldosterone response to ACTH or sodium deprivation in the subjects with panhypopituitarism. Somatotropin is not the essential pituitary hormone required for a normal aldosterone response to ACTH or sodium deprivation since a normal aldosterone response was observed in subjects with isolated GH deficiency, and growth hormone replacement therapy failed to restore a normal aldosterone response in the subjects with panhypopituitarism. (J Clin Endocrinol Metab46:247, 1978)