Discovery - University of Dundee - Online Publications

Library & Learning Centre

Ionic mechanism of forskolin-induced liquid secretion by porcine bronchi

Ionic mechanism of forskolin-induced liquid secretion by porcine bronchi

Research output: Contribution to journalArticle

View graph of relations


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

Research units


Original languageEnglish
Pages (from-to)L97-L104
JournalAmerican Journal of Physiology: Lung Cellular and Molecular Physiology
Issue number1
StatePublished - Jan 2006


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.


Library & Learning Centre

Contact | Accessibility | Policy