Journal of Clinical Endocrinology & Metabolism, Vol 56, 627-631, Copyright © 1983 by Endocrine Society

ARTICLES

Failure of angiotensin II to stimulate increases in concentrations of adrenal androgens, 17-hydroxyprogesterone, or adrenocorticotropin in congenital 21-hydroxylase deficiency

M Wisgerhof, RC Mellinger and MS Zafar

To determine if angiotensin II stimulates an increase in the plasma concentration of androstenedione, dehydroepiandrosterone, 17- hydroxyprogesterone, or ACTH in a patient with congenital 21- hydroxylase deficiency, we measured these plasma concentrations before and after the plasma angiotensin II concentration was increased by upright posture and angiotensin II infusion in a surgically castrate XX adult patient with this disorder. The patient was studied before treatment, after treatment with 1 mg dexamethasone daily for 3 weeks, and after treatment with both dexamethasone and 0.2 mg fludrocortisone daily for 3 weeks. The plasma concentrations of androstenedione, dehydroepiandrosterone, and 17-hydroxyprogesterone did not change consistently during increases in the angiotensin II concentration. The ACTH concentration did not increase in response to raised angiotensin II concentrations before or after steroid treatment. During the infusion of angiotensin II, blood pressure increased and renin activity decreased appropriate in degree to the preinfusion concentration of angiotensin II. The results from the study of this patient do not support the hypotheses that in congenital 21-hydroxylase deficiency, angiotensin II directly stimulates adrenal androgen secretion or that angiotensin II stimulates ACTH secretion.