{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,12]],"date-time":"2026-02-12T15:43:19Z","timestamp":1770910999870,"version":"3.50.1"},"reference-count":72,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2012,6,27]],"date-time":"2012-06-27T00:00:00Z","timestamp":1340755200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2012,7]]},"abstract":"<jats:p><jats:bold>BACKGROUND AND PURPOSE<\/jats:bold>The transepithelial absorption of Na<jats:sup>+<\/jats:sup>in the lungs is crucial for the maintenance of the volume and composition of epithelial lining fluid. The regulation of Na<jats:sup>+<\/jats:sup>transport is essential, because hypo\u2010 or hyperabsorption of Na<jats:sup>+<\/jats:sup>is associated with lung diseases such as pulmonary oedema or cystic fibrosis. This study investigated the effects of the gaseous signalling molecule hydrogen sulphide (H<jats:sub>2<\/jats:sub>S) on Na<jats:sup>+<\/jats:sup>absorption across pulmonary epithelial cells.<\/jats:p><jats:p><jats:bold>EXPERIMENTAL APPROACH<\/jats:bold>Ion transport processes were electrophysiologically assessed in Ussing chambers on H441 cells grown on permeable supports at air\/liquid interface and on native tracheal preparations of pigs and mice. The effects of H<jats:sub>2<\/jats:sub>S were further investigated on Na<jats:sup>+<\/jats:sup>channels expressed in<jats:italic>Xenopus<\/jats:italic>oocytes and Na<jats:sup>+<\/jats:sup>\/K<jats:sup>+<\/jats:sup>\u2010ATPase activity<jats:italic>in vitro<\/jats:italic>. Membrane abundance of Na<jats:sup>+<\/jats:sup>\/K<jats:sup>+<\/jats:sup>\u2010ATPase was determined by surface biotinylation and Western blot. Cellular ATP concentrations were measured colorimetrically, and cytosolic Ca<jats:sup>2+<\/jats:sup>concentrations were measured with Fura\u20102.<\/jats:p><jats:p><jats:bold>KEY RESULTS<\/jats:bold>H<jats:sub>2<\/jats:sub>S rapidly and reversibly inhibited Na<jats:sup>+<\/jats:sup>transport in all the models employed. H<jats:sub>2<\/jats:sub>S had no effect on Na<jats:sup>+<\/jats:sup>channels, whereas it decreased Na<jats:sup>+<\/jats:sup>\/K<jats:sup>+<\/jats:sup>\u2010ATPase currents. H<jats:sub>2<\/jats:sub>S did not affect the membrane abundance of Na<jats:sup>+<\/jats:sup>\/K<jats:sup>+<\/jats:sup>\u2010ATPase, its metabolic or calcium\u2010dependent regulation, or its direct activity. However, H<jats:sub>2<\/jats:sub>S inhibited basolateral calcium\u2010dependent K<jats:sup>+<\/jats:sup>channels, which consequently decreased Na<jats:sup>+<\/jats:sup>absorption by H441 monolayers.<\/jats:p><jats:p><jats:bold>CONCLUSIONS AND IMPLICATIONS<\/jats:bold>H<jats:sub>2<\/jats:sub>S impairs pulmonary transepithelial Na<jats:sup>+<\/jats:sup>absorption, mainly by inhibiting basolateral Ca<jats:sup>2+<\/jats:sup>\u2010dependent K<jats:sup>+<\/jats:sup>channels. These data suggest that the H<jats:sub>2<\/jats:sub>S signalling system might represent a novel pharmacological target for modifying pulmonary transepithelial Na<jats:sup>+<\/jats:sup>transport.<\/jats:p>","DOI":"10.1111\/j.1476-5381.2012.01909.x","type":"journal-article","created":{"date-parts":[[2012,2,21]],"date-time":"2012-02-21T17:28:17Z","timestamp":1329845297000},"page":"1946-1963","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":26,"title":["The gasotransmitter hydrogen sulphide decreases Na<sup>+<\/sup>transport across pulmonary epithelial 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