ADDITIVE EFFECT BETWEEN ALDOSTERONE AND INCREASED EXTRACELLULAR POTASSIUM FOR ENaC REGULATION

We have shown that potassium (K) itself acts through the master kinase mTOR within its type 2 complex (mTORC2) to activate the serum and glucocorticoid-regulated kinase 1 (SGK1), which stimulates the epithelial sodium channel (ENaC) to enhance K excretion in principal cells of cortical collecting duct (CCD); in part, by a mechanism that involves the phosphorylation of ubiquitin ligase (Nedd4-2). In the CCD, the action of aldosterone is particularly important to regulate the transcription of SGK1 and the activity of ENaC. However, the potential interconnections of these mechanisms have not been determined.