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Ionic mechanism of forskolin-induced liquid secretion by porcine bronchi

¹Department of Physiology, College of Medicine, University of South Alabama, Mobile, Alabama; and ²Maternal and Child Health Sciences, Ninewells Hospital, Dundee University, Dundee, United Kingdom

Submitted 11 April 2005 ; accepted in final form 4 August 2005

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_v) of porcine distal bronchi. The forskolin-induced J_v 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 J_v 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_v 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.

cystic fibrosis; airway liquid secretion; submucosal glands

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