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Proc Am Thorac Soc. 2004;1(1):4-9.

The epithelial sodium channel: activation by membrane-bound serine proteases.

Author information

1
Department of Pharmacology, University of Lausanne, Lausanne, Switzerland. Bernard.Rossier@ipharm.unil.ch

Abstract

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.

PMID:
16113404
DOI:
10.1513/pats.2306007
[Indexed for MEDLINE]

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