Mediators of aldosterone action in the renal tubule

The aldosterone-sensitive distal nephron extends from the second part of th e distal convoluted tubule to the inner medullary collecting duct. As recen tly shown, aldosterone increases within two hours the abundance of the alph a -subunit of the epithelial sodium channel along the entire aldosterone-se nsitive distal nephron, whereas it induces only in an initial portion of th e aldosterone-sensitive distal nephron an apical translocation of all three epithelial sodium channel subunits. This suggests that another factor or f actors determines the length of the aldosterone-sensitive distal nephron po rtion in which aldosterone controls epithelial sodium channel surface expre ssion. Since the glucocorticoid-induced kinase SGK1 was identified as aldos terone-induced protein in 1999, it has been postulated to play a key regula tory role. The in-vivo localization of its induction to segment-specific ce lls of the aldosterone-sensitive distal nephron, and the in-vitro correlati on of the amount of its hyperphosphorylated form with transepithelial sodiu m transport, support this hypothesis. Other recent studies unravel pathways other than those activated by aldosterone and insulin that impact on SGK1 expression and/or function, and thus shed some light onto the complex netwo rk that appears to control sodium transport. In view of the ongoing researc h, the question of how, and formally also whether, SGK1 acts on the epithel ial sodium channel should be resolved in the near future. Curr Opin Nephrol Hypertens 10:667-675, (C) 2001 Lippincott Williams & Wilkins.