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Adrenal Glomerulosa Function in Patients with Dexamethasone-Suppressible Hyperaldosteronism^*

Division of Pediatric Endocrinology, The New York Hospital-Cornell Medical Center New York, New York 10021
Universitäts-Kinderklinik 69 Heidelberg, West Germany
Departments of Pediatrics, Medicine, and Surgery, University of Arizona Tucson, Arizona 85724

Address requests for repints to: Dr. Sharon E. Oberfield, Division of Pediatric Endocrinology, The New York Hospital-Cornell Medical Center, 525 East 68th Street, New York, New York. 10021.

The response of the adrenal glomerulosa to renin stimulation was determined in 10 patients with dexamethasone- suppressible hyperaldosteronism. The patients were treated continuously with 2 mg%day dexamethasone (DEX) and were studied on a regular sodium diet (87 meq%m² · day) and on a 10 meq%day sodium diet. With DEX treatment all patients showed a prompt suppression of adrenal fasciculata function as evidenced by suppression of serum cortisol, corticosterone, desoxycorticosterone, and urinary 18-OH-desoxycorticosterone. The complete suppression of urinary pH 1 aldosterone (aldo) by DEX, unique to this disorder, was paralleled by a prompt suppression of urinary 18-OH-corticosterone. With continued DEX administration, plasma renin activity rose to the normal or supranormal range. Dietary sodium restriction resulted in a further rise in plasma renin activity and a rise in urinary pH 1 aldo and 18-OH-corticosterone. We conclude that in DEX-suppressible hyperaldosteronism, although ACTH appears to be the primary stimulus for aldo secretion in the untreated state, when ACTH is suppressed, the adrenal glomerulosa responds normally to the stimulation of renin-angiotensin II.

^* This research was supported in part by USPHS NIH Grant HD-00072, HL-17749, HL-18323, HL-5860, AM-6354, and by grants RR 47, and RR 0714 from the general Clinical Research Centers Program, Division of Research Resources, NIH.

Received December 22, 1980.

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