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In this study, the effects of NO on sodium reabsorption by H441 cell monolayers were studied in an Ussing chamber. Two NO donors, (Z)-1-[N-(3-aminopropyl)-N-(n-propyl)amino]diazen-1-ium-1,2-diolate and diethylammonium (Z)-1-(N,N-diethylamino)diazen-1-ium-1,2-diolate, rapidly, reversibly, and dose-dependently reduced amiloride-sensitive, short-circuit currents across H441 cell monolayers. This effect was neutralized by the NO scavenger hemoglobin and was not observed with inactive NO donors. The effects of NO were not blocked by 8-bromoguanosine-3\u2032,5\u2032-cyclic monophosphate or by soluble guanylate cyclase inhibitors (methylene blue and 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one) and were therefore independent of soluble guanylate cyclase signaling. NO targeted apical, highly selective, amiloride-sensitive Na+ channels in basolaterally permeabilized H441 cell monolayers. NO had no effect on the activity of the human epithelial sodium channel heterologously expressed in Xenopus oocytes. NO decreased Na+\/K+-ATPase activity in apically permeabilized H441 cell monolayers. The inhibition of Na+\/K+-ATPase activity by NO was reversed by mercury and was mimicked by N-ethylmaleimide, which are agents that reverse and mimic, respectively, the reaction of NO with thiol groups. Consistent with these data, S-NO groups were detected on the Na+\/K+-ATPase \u03b1 subunit in response to NO-donor application, using a biotin-switch approach coupled to a Western blot. These data demonstrate that, in the H441 cell model, NO impairs Na+ reabsorption by interfering with the activity of highly selective Na+ channels and the Na+\/K+-ATPase.<\/jats:p>","DOI":"10.1165\/2009-0335oc","type":"journal-article","created":{"date-parts":[[2010,2,5]],"date-time":"2010-02-05T21:57:30Z","timestamp":1265407050000},"page":"53-65","source":"Crossref","is-referenced-by-count":33,"title":["Nitric Oxide Inhibits Highly Selective Sodium Channels and the Na+\/K+-ATPase in H441 Cells"],"prefix":"10.1093","volume":"44","author":[{"given":"Mike","family":"Althaus","sequence":"first","affiliation":[{"name":"Institute of Animal Physiology, and"},{"name":"Department of Internal Medicine, University of Giessen Lung Center, Justus-Liebig-University, Giessen, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alexandra","family":"Pichl","sequence":"additional","affiliation":[{"name":"Institute of Animal Physiology, 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