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Titolo:
Mediators of aldosterone action in the renal tubule
Autore:
Loffing, J; Summa, V; Zecevic, M; Verrey, F;
Indirizzi:
Univ Zurich, Inst Physiol, CH-8057 Zurich, Switzerland Univ Zurich Zurich Switzerland CH-8057 siol, CH-8057 Zurich, Switzerland Univ Zurich, Inst Anat, CH-8057 Zurich, Switzerland Univ Zurich Zurich Switzerland CH-8057 Anat, CH-8057 Zurich, Switzerland
Titolo Testata:
CURRENT OPINION IN NEPHROLOGY AND HYPERTENSION
fascicolo: 5, volume: 10, anno: 2001,
pagine: 667 - 675
SICI:
1062-4821(200109)10:5<667:MOAAIT>2.0.ZU;2-B
Fonte:
ISI
Lingua:
ENG
Soggetto:
EPITHELIAL SODIUM-CHANNEL; CORTICAL COLLECTING TUBULE; INDUCIBLE PROTEIN-KINASE; TRANSCRIPTIONAL REGULATION; A6 EPITHELIA; CORTICOSTEROID REGULATION; HORMONAL-REGULATION; XENOPUS OOCYTES; DISTAL NEPHRON; ENAC SUBUNITS;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
74
Recensione:
Indirizzi per estratti:
Indirizzo: Verrey, F Univ Zurich, Inst Physiol, Winterthurerstr 190, CH-8057 Zurich, Switzerland Univ Zurich Winterthurerstr 190 Zurich Switzerland CH-8057 land
Citazione:
J. Loffing et al., "Mediators of aldosterone action in the renal tubule", CURR OP NEP, 10(5), 2001, pp. 667-675

Abstract

The aldosterone-sensitive distal nephron extends from the second part of the distal convoluted tubule to the inner medullary collecting duct. As recently shown, aldosterone increases within two hours the abundance of the alpha -subunit of the epithelial sodium channel along the entire aldosterone-sensitive distal nephron, whereas it induces only in an initial portion of the aldosterone-sensitive distal nephron an apical translocation of all three epithelial sodium channel subunits. This suggests that another factor or factors determines the length of the aldosterone-sensitive distal nephron portion in which aldosterone controls epithelial sodium channel surface expression. Since the glucocorticoid-induced kinase SGK1 was identified as aldosterone-induced protein in 1999, it has been postulated to play a key regulatory role. The in-vivo localization of its induction to segment-specific cells of the aldosterone-sensitive distal nephron, and the in-vitro correlation of the amount of its hyperphosphorylated form with transepithelial sodium transport, support this hypothesis. Other recent studies unravel pathways other than those activated by aldosterone and insulin that impact on SGK1expression and/or function, and thus shed some light onto the complex network that appears to control sodium transport. In view of the ongoing research, the question of how, and formally also whether, SGK1 acts on the epithelial sodium channel should be resolved in the near future. Curr Opin Nephrol Hypertens 10:667-675, (C) 2001 Lippincott Williams & Wilkins.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 22/09/20 alle ore 22:15:32