Cortisol as a mineralocorticoid in human disease.
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.
Department of Medicine, University of Birmingham, Queen Elizabeth Hospital, Edgbaston, England, UK.
P M
PM
Stewart
D042842:11-beta-Hydroxysteroid Dehydrogenases; D003480:Cushing Syndrome / Q000201:enzymology / Q000503:physiopathology; D006035:Glycyrrhiza; D006801:Humans; D006854:Hydrocortisone / Q000502:physiology*; D006913:Hydroxysteroid Dehydrogenases / Q000235:genetics / Q000378:metabolism; D006973:Hypertension / Q000201:enzymology / Q000378:metabolism / Q000503:physiopathology; D007674:Kidney Diseases / Q000201:enzymology / Q000378:metabolism / Q000503:physiopathology; D008901:Mineralocorticoids / Q000502:physiology*; D010946:Plants, Medicinal
D008901:Mineralocorticoids; D006913:Hydroxysteroid Dehydrogenases; D042842:11-beta-Hydroxysteroid Dehydrogenases; D006854:Hydrocortisone