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New insights into the role of serum- and glucocorticoid-inducible kinase SGK1 in the regulation of renal function and blood pressure Vallon V; Lang FCurr Opin Nephrol Hypertens 2005[Jan]; 14 (1): 59-66PURPOSE OF REVIEW: The serum and glucocorticoid inducible kinase 1 (SGK1) is induced in the aldosterone sensitive distal nephron (ASDN) where it may stimulate Na reabsorption, partly by inhibiting ubiquitin ligase Nedd4-2-mediated retrieval of epithelial Na+ channel ENaC from the luminal membrane. We describe recent advances in our understanding of SGK1 function in the regulation of renal function and blood pressure. RECENT FINDINGS: Thiazolidinediones, i.e. activators of peroxisome proliferator-activated receptor gamma (PPAR gamma), upregulate SGK1 and ENaC mRNA expression and increase cell-surface expression of ENaC alpha in a human cortical-collecting-duct cell line. cAMP/protein kinase A can induce phosphorylation and inhibition of Nedd4-2-independent of SGK1. Part of ENaC stimulation by SGK1 appears dependent on a SGK1 consensus motif in ENaC alpha and independent of Nedd4-2. SGK1-dependent upregulation of Na+ reabsorption in ASDN contributes to upregulation of renal K+ excretion. In oocytes, SGK1 activates various renal transport proteins including Na+/glucose cotransporter SGLT1, Na+-coupled dicarboxylate transporter NaDC-1, epithelial Ca+ channel TRPV5, renal outer medullary K+ channel ROMK and voltage gated K+ channels KCNE1/KCNQ1 and Kv1.3. A variant of the SGK1 gene associates with increased blood pressure and body mass index. SUMMARY: PPAR gamma activators may increase renal Na reabsorption by stimulating SGK1 and ENaC. Nedd4-2 integrates influences of cAMP/protein kinase A and SGK1. SGK1 can activate ENaC in part directly and independent of Nedd4-2. K+ homeostasis requires SGK1-dependent Na+ reabsorption in ASDN. SGK1 may affect renal transport mechanisms beyond Na+ reabsorption and K+ secretion in ASDN. Polymorphisms of SGK1 may be relevant to the pathophysiology of hypertension and other diseases.|Blood Pressure/*physiology[MESH]|Cyclic AMP-Dependent Protein Kinases/metabolism[MESH]|Humans[MESH]|Immediate-Early Proteins[MESH]|Kidney Tubules, Distal/metabolism/*physiology[MESH]|Nuclear Proteins/*metabolism[MESH]|PPAR gamma/metabolism[MESH]|Polymorphism, Genetic[MESH]|Potassium/metabolism[MESH]|Protein Serine-Threonine Kinases/*metabolism[MESH]|Sodium Channels/metabolism[MESH]|Sodium/metabolism[MESH]|Ubiquitin-Protein Ligases/metabolism[MESH]|Up-Regulation[MESH] |
