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Articles in PresS, published online ahead of print July 12, 2002
J Appl Physiol, 10.1152/jap.00413.2002
Submitted on May 10, 2002
Accepted on July 9, 2002
ENaC transgenic mice, a model for pulmonary edema
1 Institut de Pharmacologie et de Toxicologie, Universite de Lausanne, Lausanne, Switzerland
2 Institut de Pharmacologie et de Toxicologie, Universite de Lausanne, Lausanne, Switzerland; Institut de Pharmacologie et de Toxicologie, Lausanne, Switzerland
* To whom correspondence should be addressed. E-mail: ehummler{at}pop-server.unil.ch.
The amiloride-sensitive 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 mice (ENaC-/-Tg+) 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. A ~60% reduction in the baseline amiloride-sensitive sodium transport was observed, but the pharmacological characteristics and the physiological regulation of the channel was 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 down regulation of Na+ transport and ß-adrenergic stimulation was effective to stimulate sodium transport after the hypoxia-induced decrease. When down regulation of ENaC activity (such as observed under hypoxia) is added to a low "constitutive" ENaC expression, the resulting reduced sodium transport rate may be insufficient for airway fluid clearance and favor pulmonary edema.
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