Forms of mineralocorticoid hypertension.

Détails

ID Serval
serval:BIB_D83AD31DC006
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
Forms of mineralocorticoid hypertension.
Périodique
Vitamins and Hormones
Auteur(s)
Ferrari P., Bonny O.
ISSN
0083-6729 (Print)
ISSN-L
0083-6729
Statut éditorial
Publié
Date de publication
2003
Peer-reviewed
Oui
Volume
66
Pages
113-156
Langue
anglais
Résumé
Hypertension with hypokalemia, metabolic alkalosis, and suppressed plasma renin activity defines mineralocorticoid hypertension. Mineralocorticoid hypertension is the consequence of an overactivity of the epithelial sodium channel expressed at the apical membrane of renal cells in the distal nephron. This is usually the case when the mineralocorticoid receptor is activated by its physiologic substrate aldosterone. The best known form of mineralocorticoid hypertension is an aldosterone-producing adrenal tumor leading to primary aldosteronism. Primary aldosteronism can also be caused by unilateral or bilateral adrenal hyperplasia and rarely adrenal carcinoma. Interestingly, most of the inherited monogenic disorders associated with hypertension involve an excessive activation of the mineralocorticoid axis. In some of these disorders, mineralocorticoid hypertension results from activation of the mineralocorticoid receptor by other steroids (cortisol, deoxycorticosterone), by primary activation of the receptor itself, or by constitutive overactivity of the renal epithelial sodium channel. The present review addresses the physiology and significance of the key players of the mineralocorticoid axis, placing emphasis on the conditions leading to mineralocorticoid hypertension.
Mots-clé
11-beta-Hydroxysteroid Dehydrogenase Type 2, Adrenal Gland Neoplasms/complications, Adrenocortical Hyperfunction/complications, Aldosterone/pharmacology, Aldosterone/physiology, Aldosterone Synthase/genetics, Animals, Humans, Hydroxysteroid Dehydrogenases/genetics, Hyperaldosteronism/complications, Hyperaldosteronism/diagnosis, Hypertension/etiology, Hypertension/genetics, Mineralocorticoids, Mutation, Receptors, Mineralocorticoid/drug effects, Receptors, Mineralocorticoid/genetics, Renin-Angiotensin System, Sodium Channels/genetics
Pubmed
Création de la notice
01/02/2010 12:28
Dernière modification de la notice
03/03/2018 21:50
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