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.

• Authors: P M Stewart
• Journal: The 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
• PMID: 10419018 (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