Mechanisms of aldosterone's action on epithelial Na + transport

• Published in: The Journal of membrane biology Vol. 184; no. 3; pp. 313 - 319
• Main Authors: Eaton, D C, Malik, B, Saxena, N C, Al-Khalili, O K, Yue, G
• Format: Journal Article
• Language: English
• Published: United States Springer Nature B.V 01-12-2001
• Subjects: Aldosterone; Aldosterone - metabolism; Aldosterone - pharmacology; Aldosterone - physiology; Animals; Anura; Biological Transport - physiology; Cell Membrane - physiology; Electric Conductivity; Epithelial Cells - drug effects; Epithelial Cells - metabolism; Epithelial Sodium Channels; GTP-Binding Proteins - genetics; GTP-Binding Proteins - metabolism; Patch-Clamp Techniques - methods; Sodium - pharmacokinetics; Sodium Channels - pharmacokinetics; Sodium Channels - pharmacology; Sodium-Potassium-Exchanging ATPase - physiology
• ISSN: 0022-2631; 1432-1424
• DOI: 10.1007/s00232-001-0098-x

Aldosterone maintains total organism sodium balance in all higher vertebrates. The level of sodium reabsorption is primarily determined by the action of aldosterone on epithelial sodium channels (ENaC) in the distal nephron. Recent work shows that, in an aldosterone-sensitive renal cell line (A6), aldosterone regulates sodium reabsorption by short- and long-term processes. In the short term, aldosterone regulates sodium transport by inducing expression of the small G-protein, K-Ras2A, by stimulating the activity of methyl transferase and S-adenosyl-homocysteine hydrolase to activate Ras by methylation, and, possibly, by subsequent activation by K-Ras2A of phosphatidylinositol phosphate-5-kinase (PIP-5-K) and phosphatidylinositol-3-kinase (PI-3-K), which ultimately activates ENaC. In the long term, aldosterone regulates sodium transport by altering trafficking, assembly, and degradation of ENaC.