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Cortisol as a mineralocorticoid in human disease.

Abstract
The type 2 isozyme of 11beta-hydroxysteroid dehydrogenase inactivates cortisol to cortisone and enables aldosterone to bind to the MR. Congenital deficiency of the enzyme results in cortisol-mediated mineralocorticoid excess and arises because of inactivating mutations in the HSD11B2 gene. Inhibition of the enzyme following licorice or carbenoxolone ingestion results in a similar, though milder phenotype and the enzyme is overwhelmed in ectopic ACTH syndrome. Loss of 11beta-HSD2 expression may be important in sodium balance and blood pressure control in some patients with renal disease. Finally, while some studies demonstrate impaired 11beta-HSD activity in broader populations of patients with hypertension, further studies are required to clarify the role of 11beta-HSD2 in 'essential' hypertension.
AuthorsP M Stewart
JournalThe Journal of steroid biochemistry and molecular biology (J Steroid Biochem Mol Biol) 1999 Apr-Jun Vol. 69 Issue 1-6 Pg. 403-8 ISSN: 0960-0760 [Print] ENGLAND
PMID10419018 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
Chemical References
  • Mineralocorticoids
  • Hydroxysteroid Dehydrogenases
  • 11-beta-Hydroxysteroid Dehydrogenases
  • Hydrocortisone
Topics
  • 11-beta-Hydroxysteroid Dehydrogenases
  • Cushing Syndrome (enzymology, physiopathology)
  • Glycyrrhiza
  • Humans
  • Hydrocortisone (physiology)
  • Hydroxysteroid Dehydrogenases (genetics, metabolism)
  • Hypertension (enzymology, metabolism, physiopathology)
  • Kidney Diseases (enzymology, metabolism, physiopathology)
  • Mineralocorticoids (physiology)
  • Plants, Medicinal

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