Ionic mechanism of forskolin-induced liquid secretion by porcine bronchi

Stephen T. Ballard, Laura Trout, Jennifer Garrison, Sarah Inglis

    Research output: Contribution to journalArticle

    21 Citations (Scopus)

    Abstract

    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 (Jv) of porcine distal bronchi. The forskolin-induced Jv was driven by a combination of bumetanide-sensitive Cl– secretion and DIDS-sensitive HCO3– secretion. When Cl– secretion was inhibited with bumetanide, Na+/H+ exchange-dependent HCO3– secretion was apparently induced to compensate for the loss of Cl– secretion. The forskolin-induced Jv 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 Jv 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+-HCO3– cotransporter or an Na+-dependent anion exchanger, which could account for transepithelial HCO3– secretion.
    Original languageEnglish
    Pages (from-to)L97-L104
    JournalAmerican Journal of Physiology: Lung Cellular and Molecular Physiology
    Volume290
    Issue number1
    Publication statusPublished - Jan 2006

    Keywords

    • Cystic fibrosis
    • Airway liquid secretion
    • Submucosal glands

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