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© 2004 The American Thoracic Society
The Epithelial Sodium Channel
Activation by Membrane-Bound Serine Proteases
Departments of Pharmacology and of Toxicology, University of Lausanne, Lausanne, Switzerland
Correspondence and requests for reprints should be addressed to Bernard C. Rossier, M.D., Bugnon 27, CH-1005-Lausanne, Switzerland. E-mail: Bernard.Rossier{at}ipharm.unil.ch
The epithelial sodium channel (ENaC) was cloned just 10 years ago. Since that time, the study of human monogenic diseases (pseudohypoaldosteronism type 1 [PHA-1] and Liddle syndrome), as well as mouse models mimicking salt-losing syndromes (PHA-1) or salt-sensitive hypertension (Liddle syndrome), have greatly contributed to our understanding of the function of ENaC in vivo. In this brief review, I will first discuss ENaC as a limiting factor in the control of ionic composition of the extracellular fluid and then, more specifically, the activation of ENaC by membrane-bound serine proteases. Recent in vitro and in vivo experiments indicate that membrane-bound serine proteases (channel activating proteases [CAP-1, -2, or-3]) may be of critical importance in the activation of ENaC in different organs, such as the kidney, the lung or the cochlea.
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