{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T17:05:31Z","timestamp":1791219931625,"version":"4.1.0"},"reference-count":49,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2007,7,5]],"date-time":"2007-07-05T00:00:00Z","timestamp":1183593600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2007,7,15]]},"abstract":"<jats:p>Transepithelial sodium transport via alveolar epithelial Na<jats:sup>+<\/jats:sup> channels and Na<jats:sup>+<\/jats:sup>,K<jats:sup>+<\/jats:sup>\u2010ATPase constitutes the driving force for removal of alveolar oedema fluid. Decreased activity of the amiloride\u2010sensitive epithelial Na<jats:sup>+<\/jats:sup> channel (ENaC) in the apical membrane of alveolar epithelial cells impairs sodium\u2010driven alveolar fluid clearance (AFC) and predisposes to pulmonary oedema. We hypothesized that hyperactivity of ENaC in the distal lung could improve AFC and facilitate the resolution of pulmonary oedema. AFC and lung fluid balance were studied at baseline and under conditions of hydrostatic pulmonary oedema in the \u03b2\u2010Liddle (L) mouse strain harbouring a gain\u2010of\u2010function mutation (R<jats:sup>566<\/jats:sup><jats:sub>stop<\/jats:sub>) within the <jats:italic>Scnn1b<\/jats:italic> gene. As compared with wild\u2010type (+\/+), baseline AFC was increased by 2\u2010 and 3\u2010fold in heterozygous (+\/L) and homozygous mutated (L\/L) mice, respectively, mainly due to increased amiloride\u2010sensitive AFC. The \u03b2<jats:sub>2<\/jats:sub>\u2010agonist terbutaline stimulated AFC in +\/+ and +\/L mice, but not in L\/L mice. Acute volume overload induced by saline infusion (40% of body weight over 2 h) significantly increased extravascular (i.e. interstitial and alveolar) lung water as assessed by the bloodless wet\u2010to\u2010dry lung weight ratio in +\/+ and L\/L mice, as compared with baseline. However, the increase was significantly larger in +\/+ than in L\/L groups (<jats:italic>P<\/jats:italic>= 0.01). Volume overload also increased the volume of the alveolar epithelial lining fluid in +\/+ mice, indicating the presence of alveolar oedema, but not in L\/L mice. Cardiac function as evaluated by echocardiography was comparable in both groups. These data show that constitutive ENaC activation improved sodium\u2010driven AFC in the mouse lung, and attenuated the severity of hydrostatic pulmonary oedema.<\/jats:p>","DOI":"10.1113\/jphysiol.2007.131078","type":"journal-article","created":{"date-parts":[[2007,4,13]],"date-time":"2007-04-13T00:24:24Z","timestamp":1176423864000},"page":"777-788","source":"Crossref","is-referenced-by-count":30,"title":["\u03b2\u2010Liddle mutation of the epithelial sodium channel increases alveolar fluid clearance and reduces the severity of hydrostatic pulmonary oedema in 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