{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,19]],"date-time":"2025-10-19T05:52:34Z","timestamp":1760853154432},"reference-count":59,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2006,6,7]],"date-time":"2006-06-07T00:00:00Z","timestamp":1149638400000},"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":[[2006,6,15]]},"abstract":"The duodenum is the site of mixing of massive amounts of gastric H+<\/jats:sup> with secreted HCO3<\/jats:sub>\u2212<\/jats:sup>, generating CO2<\/jats:sub> and H2<\/jats:sub>O accompanied by the neutralization of H+<\/jats:sup>. We examined the role of membrane\u2010bound and soluble carbonic anhydrases (CA) by which H+<\/jats:sup> is neutralized, CO2<\/jats:sub> is absorbed, and HCO3<\/jats:sub>\u2212<\/jats:sup> is secreted. Rat duodena were perfused with solutions of different pH and P<\/jats:italic><\/jats:styled-content> with or without a cell\u2010permeant CA inhibitor methazolamide (MTZ) or impermeant CA inhibitors. Flow\u2010through pH and P<\/jats:italic><\/jats:styled-content> electrodes simultaneously measured perfusate and effluent pH and P<\/jats:italic><\/jats:styled-content>. High CO2<\/jats:sub> (34.7 kPa) perfusion increased net CO2<\/jats:sub> loss from the perfusate compared with controls (pH 6.4 saline, P<\/jats:italic>\u2248 0<\/jats:styled-content>) accompanied by portal venous (PV) acidification and P<\/jats:italic><\/jats:styled-content> increase. Impermeant CA inhibitors abolished net perfusate CO2<\/jats:sub> loss and increased net HCO3<\/jats:sub>\u2212<\/jats:sup> gain, whereas all CA inhibitors inhibited PV acidification and P<\/jats:italic><\/jats:styled-content> increase. The changes in luminal and PV pH and [CO2<\/jats:sub>] were also inhibited by the Na+<\/jats:sup>\u2013H+<\/jats:sup> exchanger\u20101 (NHE1) inhibitor dimethylamiloride, but not by the NHE3 inhibitor S3226. Luminal acid decreased total CO2<\/jats:sub> output and increased H+<\/jats:sup> loss with PV acidification and P<\/jats:italic><\/jats:styled-content> increase, all inhibited by all CA inhibitors. During perfusion of a 30% CO2<\/jats:sub> buffer, loss of CO2<\/jats:sub> from the lumen was CA dependent as was transepithelial transport of perfused 13<\/jats:sup>CO2<\/jats:sub>. H+<\/jats:sup> and CO2<\/jats:sub> loss from the perfusate were accompanied by increases of PV H+<\/jats:sup> and tracer CO2<\/jats:sub>, but unchanged PV total CO2<\/jats:sub>, consistent with CA\u2010dependent transmucosal H+<\/jats:sup> and CO2<\/jats:sub> movement. Inhibition of membrane\u2010bound CAs augments the apparent rate of net basal HCO3<\/jats:sub>\u2212<\/jats:sup> secretion. Luminal H+<\/jats:sup> traverses the apical membrane as CO2<\/jats:sub>, is converted back to cytosolic H+<\/jats:sup>, which is extruded via NHE1. Membrane\u2010bound and cytosolic CAs cooperatively facilitate secretion of HCO3<\/jats:sub>\u2212<\/jats:sup> into the lumen and CO2<\/jats:sub> diffusion into duodenal mucosa, serving as important acid\u2013base regulators.<\/jats:p>","DOI":"10.1113\/jphysiol.2006.107581","type":"journal-article","created":{"date-parts":[[2006,3,24]],"date-time":"2006-03-24T01:33:55Z","timestamp":1143164035000},"page":"827-842","source":"Crossref","is-referenced-by-count":50,"title":["Epithelial carbonic anhydrases facilitate P<\/i>CO2<\/sub> and pH regulation in rat duodenal 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