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-ENaC transgenic mice: a model for
pulmonary edema
1 Institut de Pharmacologie et de Toxicologie, Université de Lausanne, CH-1005 Lausanne; 2 Département de Médecine Interne, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland
The amiloride-sensitive epithelial
Na+ channel (ENaC) is essential for fluid clearance from
the airways. An experimental animal model with a reduced expression of
ENaC, the 
-ENaC transgenic rescue mouse, is prone to develop edema
under hypoxia exposure. This strongly suggests an involvement of ENaC
in the pathogenesis of pulmonary edema. To investigate the pathogenesis
of this type of edema, primary cultures of tracheal cells from these
mice were studied in vitro. An ~60% reduction in baseline
amiloride-sensitive Na+ transport was observed, but the
pharmacological characteristics and physiological regulation of the
channel were similar to those observed in cells from wild-type mice.
Aprotinin, an inhibitor of serine proteases, blocked 50-60% of
the basal transepithelial current, hypoxia induced downregulation of
Na+ transport, and 
-adrenergic stimulation was effective
to stimulate Na+ transport after the hypoxia-induced
decrease. When downregulation of ENaC activity (such as observed under
hypoxia) is added to a low "constitutive" ENaC expression, the
resulting reduced Na+ transport rate may be insufficient
for airway fluid clearance and favor pulmonary edema.
epithelial sodium channel; sodium channel; mouse model; gene targeting; transgenic; Scnn1a
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