Details

Autor(en) / Beteiligte

• Ballard, Stephen T
• Trout, Laura
• Garrison, Jennifer
• Inglis, Sarah K

Titel

Ionic mechanism of forskolin-induced liquid secretion by porcine bronchi

Ist Teil von

• American journal of physiology. Lung cellular and molecular physiology, 2006-01, Vol.290 (1), p.L97-L104

Ort / Verlag

United States

Erscheinungsjahr

2006

Quelle

Free E-Journal (出版社公開部分のみ）

Beschreibungen/Notizen

• 1 Department of Physiology, College of Medicine, University of South Alabama, Mobile, Alabama; and 2 Maternal 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 HCO 3 – secretion. When Cl – secretion was inhibited with bumetanide, Na + /H + exchange-dependent HCO 3 – 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 + -HCO 3 – cotransporter or an Na + -dependent anion exchanger, which could account for transepithelial HCO 3 – secretion. cystic fibrosis; airway liquid secretion; submucosal glands Address for reprint requests and other correspondence: S. T. Ballard, Dept. of Physiology, MSB 3074, Univ. of South Alabama, Mobile, AL 36688 (e-mail: sballard{at}usouthal.edu )