Document Detail


Cortisol, 11beta-hydroxysteroid dehydrogenases, and hypertension.
MedLine Citation:
PMID:  15478032     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Hypersecretion of cortisol is associated with hypertension. In addition, an abnormal cortisol metabolism may play a role in the pathogenesis of hypertension. The 11beta-hydroxysteroid dehydrogenase (11beta-HSD) isozymes catalyze interconversion of cortisol and cortisone and play an important role in the regulation of the effects of cortisol. Activity of 11beta-HSD type 2, converting active cortisol in inactive cortisone, is crucial in preventing access of cortisol to the renal mineralocorticoid receptors (MRs). Decreased activity of this isozyme in the kidney, either congenitally in Apparent Mineralocorticoid Excess syndrome or acquired following licorice consumption, allows cortisol access to the MRs, resulting in hypokalemic hypertension. In normotensive subjects, an association has been demonstrated between blood pressure increase on a high-salt diet and a mild decrease of renal 11beta-HSD2 activity. In ectopic adrenocorticotropic hormone (ACTH), plasma cortisol levels are very high, resulting in mineralocorticoid hypertension caused by saturation of the available renal 11beta-HSD2 capacity. Activity of the 11beta-HSDs has also been demonstrated in many extrarenal sites. Several studies have demonstrated extrarenal effects of cortisol on blood pressure, as well as a possible role for altered extrarenal 11beta-HSD activities in the pathogenesis of hypertension. More studies are needed to clarify the role of 11beta-HSDs in the pathogenesis of hypertension.
Authors:
Stan H M van Uum; Jacques W M Lenders; Ad R M M Hermus
Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Seminars in vascular medicine     Volume:  4     ISSN:  1528-9648     ISO Abbreviation:  Semin Vasc Med     Publication Date:  2004 May 
Date Detail:
Created Date:  2004-10-12     Completed Date:  2005-02-08     Revised Date:  2005-11-16    
Medline Journal Info:
Nlm Unique ID:  100940307     Medline TA:  Semin Vasc Med     Country:  United States    
Other Details:
Languages:  eng     Pagination:  121-8     Citation Subset:  IM    
Affiliation:
Division of Endocrinology and Metabolism, Department of Medicine, University of Western Ontario, London, Ontario, Canada.
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MeSH Terms
Descriptor/Qualifier:
11-beta-Hydroxysteroid Dehydrogenases / physiology*
Animals
Blood Pressure / physiology
Cushing Syndrome / physiopathology
Fetus / physiology
Glycyrrhiza
Humans
Hydrocortisone / blood*,  secretion
Hypertension / blood,  physiopathology*
Hypertension, Renal / blood,  physiopathology
Kidney / physiopathology
Kidney Failure, Chronic / physiopathology
Placenta / physiology
Receptors, Mineralocorticoid / physiology
Chemical
Reg. No./Substance:
0/Receptors, Mineralocorticoid; 50-23-7/Hydrocortisone; EC 1.1.1.146/11-beta-Hydroxysteroid Dehydrogenases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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