Adrenal glomerulosa function in patients with dexamethasone-suppressible hyperaldosteronism

Sharon E. Oberfield, Lenore S. Levine, Elizabeth Stoner, Diane Chow, Wolfgang Rauh, Fenella Greig, Stanley M. Lee, Elmer Lightner, Marlys Witte, Maria I. New

Research output: Contribution to journalArticlepeer-review

52 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)158-164
Number of pages7
JournalJournal of Clinical Endocrinology and Metabolism
Issue number1
StatePublished - Jul 1981

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Biochemistry
  • Endocrinology
  • Clinical Biochemistry
  • Biochemistry, medical


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