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Am J Physiol Gastrointest Liver Physiol 276: G567-G571, 1999;
0193-1857/99 $5.00
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Vol. 276, Issue 3, G567-G571, March 1999

THEMES
Genetic Disorders of Membrane Transport
V. The epithelial sodium channel and its implication in human diseases*

Edith Hummler and Jean-Daniel Horisberger

Institut de Pharmacologie et de Toxicologie, Université de Lausanne, CH-1005 Lausanne, Switzerland

The epithelial Na+ channel (ENaC) controls the rate-limiting step in the process of transepithelial Na+ reabsorption in the distal nephron, the distal colon, and the airways. Hereditary salt-losing syndromes have been ascribed to loss of function mutations in the alpha -, beta -, or gamma -ENaC subunit genes, whereas gain of function mutations (located in the COOH terminus of the beta - or gamma -subunit) result in hypertension due to Na+ retention (Liddle's syndrome). In mice, gene-targeting experiments have shown that, in addition to the kidney salt-wasting phenotype, ENaC was essential for lung fluid clearance in newborn mice. Disruption of the alpha -subunit resulted in a complete abolition of ENaC-mediated Na+ transport, whereas knockout of the beta - or gamma -subunit had only minor effects on fluid clearance in lung. Disruption of each of the three subunits resulted in a salt-wasting syndrome similar to that observed in humans.

hypertension; pseudohypoaldosteronism; transgenic mice

* Fifth in a series of invited articles on Genetic Disorders of Membrane Transport.




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