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Am J Physiol Renal Physiol (May 28, 2008). doi:10.1152/ajprenal.90248.2008
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Submitted on April 12, 2008
Revised on May 12, 2008
Accepted on May 27, 2008

Regulation of the epithelial sodium channel (ENaC) by membrane trafficking

Michael Bruce Butterworth1*, Robert S. Edinger1, Raymond A. Frizzell1, and John P. Johnson1

1 University of Pittsburgh

* To whom correspondence should be addressed. E-mail: michael7{at}pitt.edu.

The epithelial Na+ channel (ENaC) is a major regulator of salt and water reabsorption in a number of epithelial tissues. Abnormalities in ENaC function have been directly linked to several human disease states including Liddle's Syndrome, psuedohypoaldosteronism and cystic fibrosis, and may be implicated in states as diverse as salt-sensitive hypertension, nephrosis, and pulmonary edema. ENaC activity in epithelial cells is highly regulated both by open probability and number of channels. Open probability is regulated by a number of factors, including proteolytic processing while ENaC number is regulated by cellular trafficking. This review discusses current understanding of apical membrane delivery, cell surface stability, endocytosis, retrieval and recycling of ENaC and the molecular partners which have so far been shown to participate in these processes. We review known sites and mechanisms of hormonal regulation of trafficking by aldosterone, vasopressin and insulin. While many details of the regulation of ENaC trafficking remain to be elucidated, knowledge of these mechanisms may provide further insights into ENaC activity in normal and disease states.




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