When is cortisol a mineralocorticoid?

Kidney Int. 1992 Dec;42(6):1297-308. doi: 10.1038/ki.1992.421.


(1) Decreased 11 beta-OHSD activity permits binding of cortisol to the Type I (mineralocorticoid) receptor in humans, thereby producing spironolactone-inhibitable Na+ retention, hypokalemia and hypertension, the syndrome of apparent mineralocorticoid excess (AME). (2) Blockade of either the Type I receptor with spironolactone or the Type II (glucocorticoid) receptor with RU-486 does not consistently abolish the effects of stress level cortisol on Na+ retention and hypertension in acute studies in normal humans, suggesting the existence of an additional glucocorticoid receptor. (3) Enhanced glucocorticoid 6 beta-hydroxylation could play an etiologic role in certain hypertensive syndromes. (4) Both decreased 11 beta-OHSD and increased 6 beta-OHase are candidates as intermediate phenotypes for the remote phenotype essential hypertension.

Publication types

  • Editorial
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • 11-beta-Hydroxysteroid Dehydrogenases
  • Animals
  • Glucocorticoids / physiology
  • Humans
  • Hydrocortisone / physiology*
  • Hydroxysteroid Dehydrogenases / deficiency
  • Hypertension / etiology
  • Hypertension / physiopathology
  • Mineralocorticoids / physiology*
  • Receptors, Glucocorticoid / physiology


  • Glucocorticoids
  • Mineralocorticoids
  • Receptors, Glucocorticoid
  • Hydroxysteroid Dehydrogenases
  • 11-beta-Hydroxysteroid Dehydrogenases
  • Hydrocortisone