{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,7]],"date-time":"2026-03-07T15:00:02Z","timestamp":1772895602076,"version":"3.50.1"},"reference-count":31,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Lung Cellular and Molecular Physiology"],"published-print":{"date-parts":[[2006,1]]},"abstract":"<jats:p>cAMP-elevating agents such as forskolin and vasoactive intestinal peptide induce liquid secretion by tracheobronchial submucosal glands. This pathway is thought to be CFTR dependent and thus defective in cystic fibrosis; however, the ionic mechanism that drives this secretion process is incompletely understood. To better define this mechanism, we studied the effects of ion transport inhibitors on the forskolin-induced liquid secretion response (J<jats:sub>v<\/jats:sub>) of porcine distal bronchi. The forskolin-induced J<jats:sub>v<\/jats:sub>was driven by a combination of bumetanide-sensitive Cl<jats:sup>\u2212<\/jats:sup>secretion and DIDS-sensitive HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>secretion. When Cl<jats:sup>\u2212<\/jats:sup>secretion was inhibited with bumetanide, Na<jats:sup>+<\/jats:sup>\/H<jats:sup>+<\/jats:sup>exchange-dependent HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>secretion was apparently induced to compensate for the loss of Cl<jats:sup>\u2212<\/jats:sup>secretion. The forskolin-induced J<jats:sub>v<\/jats:sub>was significantly inhibited by the anion channel blockers 5-nitro-2-(3-phenylpropylamino)benzoic acid, diphenylamine-2-carboxylate, and glibenclamide. We conclude that the forskolin-induced J<jats:sub>v<\/jats:sub>shares many characteristics of cholinergically induced secretion except for the presence of a DIDS-sensitive component. Although the identity of the DIDS-sensitive component is unclear, we speculate that it represents a basolateral membrane Na<jats:sup>+<\/jats:sup>-HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>cotransporter or an Na<jats:sup>+<\/jats:sup>-dependent anion exchanger, which could account for transepithelial HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>secretion.<\/jats:p>","DOI":"10.1152\/ajplung.00159.2005","type":"journal-article","created":{"date-parts":[[2005,9,24]],"date-time":"2005-09-24T00:24:37Z","timestamp":1127521477000},"page":"L97-L104","source":"Crossref","is-referenced-by-count":23,"title":["Ionic mechanism of forskolin-induced liquid secretion by porcine bronchi"],"prefix":"10.1152","volume":"290","author":[{"given":"Stephen 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