Aldosterone regulation of gene transcription leading to control of ion transport

Détails

ID Serval
serval:BIB_4129052DCAEF
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Titre
Aldosterone regulation of gene transcription leading to control of ion transport
Périodique
Hypertension
Auteur(s)
Horisberger  J. D., Rossier  B. C.
ISSN
0194-911X (Print)
Statut éditorial
Publié
Date de publication
03/1992
Volume
19
Numéro
3
Pages
221-7
Notes
Journal Article
Research Support, Non-U.S. Gov't
Review --- Old month value: Mar
Résumé
Aldosterone, like other steroid hormones, initiates its effects by binding to intracellular receptors; these receptors are then able to control the transcription of several genes. The products of these genes eventually modulate the activity of ionic transport systems located in the apical and the basolateral membrane of specialized epithelial cells, thereby modulating the excretion of Na+ and K+ ions. Considerable progress has been made recently in understanding these mechanisms and the structure of the proteins involved in these processes. A novel principle has been discovered to explain the selective effect of aldosterone on its target epithelia. These tissues exclude competing glucocorticoid hormones by the activity of the 11 beta-hydroxysteroid dehydrogenase to allow aldosterone, an enzyme-resistant steroid, to bind to its receptors. Aldosterone induces numerous changes in the activity of membrane ion transport systems and enzymes and cell morphology. Although the enhancement of Na,K-ATPase synthesis and the increase of the number of active Na+ channels in the apical membrane appear as both direct and primary effects, the mechanisms of the other effects remain to be determined. The knowledge of the primary structure of several elements of the aldosterone response system (e.g., mineralocorticoid receptor and Na,K-ATPase) allows us to understand abnormal regulation of Na+ balance at the molecular level and, potentially, to identify genetic alterations responsible for these defects.
Mots-clé
Aldosterone/*pharmacology Biological Transport/drug effects Colon/physiology Hypertension/genetics Ion Channels/drug effects Kidney/physiology Na(+)-K(+)-Exchanging ATPase/genetics Potassium/*metabolism Receptors, Aldosterone Receptors, Glucocorticoid/*genetics Sodium/*metabolism Transcription, Genetic/*drug effects
Pubmed
Web of science
Création de la notice
24/01/2008 13:38
Dernière modification de la notice
03/03/2018 16:31
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