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11-{beta} hydroxysteroid dehydrogenase-2 and salt-sensitive hypertension

Official URL:https://doi.org/10.1161/CIRCULATIONAHA.116.022038
PubMed:View item in PubMed
Creators Name:Luft, F.C.
Journal Title:Circulation
Journal Abbreviation:Circulation
Page Range:1335-1337
Date:5 April 2016
Keywords:Hypertension, Genetics, Animal Models, Genetics, Knockout Models, Animals
Abstract:Glucocorticoid intracellular metabolism, catalyzed by the two isozymes of 11 {beta}-hydroxysteroid dehydrogenase (11 {beta}-HSD), determines the corticosteroid action on target tissues.1 11 {beta}-HSD1 functions as a reductase in most cells and catalyzes the regeneration of active glucocorticoids thereby amplifying their action. This isozyme is wildely expressed in liver, adipose tissue, muscle, pancreatic islets, and adult brain. 11 {beta}-HSD2 is a high-affinity dehydrogenase and inactivates cortisol and corticosterone to the inert product, cortisone. Cortisone in turn can be reactivated through reduction by 11 {beta}-HSD1 (Figure 1). The 11 {beta}-HSD2 isozyme is highly expressed in the distal nephron and, as we learn here, in the nucleus tractus solitarius (NTS). 11 {beta}-HSD2 serves to protect the mineralocorticoid receptor (MR) from occupation by cortisol or corticosterone (Figure 2).
Publisher:American Heart Association (U.S.A.)
Item Type:Editorial

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