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| Item Type: | Editorial |
|---|---|
| Title: | 11-β hydroxysteroid dehydrogenase-2 and salt-sensitive hypertension |
| Creators Name: | Luft, F.C. |
| 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). |
| Keywords: | Hypertension, Genetics, Animal Models, Genetics, Knockout Models, Animals |
| Source: | Circulation |
| ISSN: | 0009-7322 |
| Publisher: | American Heart Association |
| Volume: | 133 |
| Number: | 14 |
| Page Range: | 1335-1337 |
| Date: | 5 April 2016 |
| Additional Information: | Copyright © 2016 American Heart Association, Inc. |
| Official Publication: | https://doi.org/10.1161/CIRCULATIONAHA.116.022038 |
| PubMed: | View item in PubMed |
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