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Am J Physiol Renal Physiol (May 23, 2006). doi:10.1152/ajprenal.00061.2006
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Submitted on February 22, 2006
Accepted on May 8, 2006

Disinhibitory Pathways for Control of Sodium Transport: Regulation of ENaC by SGK1 and GILZ

Vivek Bhalla1, Rama Soundararajan1, Alan C Pao1, Hongyan Li2, and David Pearce1*

1 Medicine, University of California, San Francisco, San Francisco, California, United States
2 Dermatology, University of California, San Francisco, San Francisco, California, United States

* To whom correspondence should be addressed. E-mail: pearce{at}medicine.ucsf.edu.

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.




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