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Am J Physiol Renal Physiol 291: F714-F721, 2006. First published May 23, 2006; doi:10.1152/ajprenal.00061.2006
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INVITED REVIEW

Disinhibitory pathways for control of sodium transport: regulation of ENaC by SGK1 and GILZ

Vivek Bhalla,1,* Rama Soundararajan,1,* Alan C. Pao,2 Hongyan Li,2 and David Pearce1

1Division of Nephrology, Department of Medicine, and 2Department of Dermatology, University of California, San Francisco, California

Regulation of ENaC occurs at several levels. The principal hormonal regulator of ENaC, aldosterone, acts through the mineralocorticoid receptor to modulate ENaC-mediated sodium transport, and considerable attention has focused on defining the components of the early phase of this response. Two genes, SGK1 and GILZ, have now been implicated in this regulation. While the functional significance of SGK1 in mediating aldosterone effects is well established, new evidence has enhanced our understanding of the mechanisms of SGK1 action. In addition, recent work demonstrates a novel role for GILZ in the stimulation of ENaC-mediated sodium transport. Interestingly, both SGK1 and GILZ appear to negatively regulate tonic inhibition of ENaC and thus use disinhibition to propagate the rapid effects of aldosterone to increase sodium reabsorption in tight epithelia.

epithelial sodium channel; Nedd4-2; 14-3-3; ERK; trafficking


Address for reprint requests and other correspondence: D. Pearce, Univ. of California San Francisco, 600 16th St., Rm. N272C, Genentech Hall, Mission Bay, Box 2140, San Francisco, CA 94107-2140 (e-mail: pearce{at}medicine.ucsf.edu)




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