Apparent mineralocorticoid excess, 11beta hydroxysteroid dehydrogenase and aldosterone action Closing one loop, opening another.
Trends Endocrinol Metab
; 6(7): 248-51, 1995 Sep.
Article
em En
| MEDLINE
| ID: mdl-18406708
ABSTRACT
The recent cloning of the human enzyme 11beta hydroxysteroid dehydrogenase type 2 (11betaHSD2), and the demonstration of point mutations or deletions in both familial and apparently sporadic cases of apparent mineralocorticoid excess (AME), underlines the importance of this enzyme in excluding glucocorticoids from mineralocorticoid receptors (MR). Although the sodium retention characteristic of AME can thus be explained by absent or very reduced (< 10%) levels of renal 11 betaHSD2 activity, whether or not the enzymatic defect contributes to the elevated blood pressure by mechanisms other than sodium retention remains to be determined.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Idioma:
En
Revista:
Trends Endocrinol Metab
Assunto da revista:
ENDOCRINOLOGIA
/
METABOLISMO
Ano de publicação:
1995
Tipo de documento:
Article
País de afiliação:
Austrália