AJP - Lung Journal of Applied Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 QUICK SEARCH:   [advanced]


     


Am J Physiol Lung Cell Mol Physiol (September 23, 2005). doi:10.1152/ajplung.00159.2005
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
290/1/L97    most recent
00159.2005v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ballard, S. T
Right arrow Articles by Inglis, S. K
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ballard, S. T
Right arrow Articles by Inglis, S. K
Submitted on April 11, 2005
Accepted on August 4, 2005

IONIC MECHANISM OF FORSKOLIN-INDUCED LIQUID SECRETION BY PORCINE BRONCHI

Stephen T Ballard1*, Laura Trout1, Jennifer Garrison1, and Sarah K Inglis2

1 Department of Physiology, University of South Alabama, Mobile, AL, USA
2 Ninewells Hospital Department of Maternal and Child Health Sciences, Dundee University, Dundee, Scotland, United Kingdom

* To whom correspondence should be addressed. E-mail: sballard{at}usouthal.edu.

cAMP-elevating agents such as forskolin and vasoactive intestinal peptide (VIP) 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 C1- secretion was inhibited with bumetanide, Na+/H+ exchange (NHE)-dependent HCO3- secretion was apparently induced to compensate for the loss of C1- secretion. The forskolin-induced Jv was significantly inhibited by the anion channel blockers NPPB, DPC, 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. While the identity of the DIDS-sensitive component is unclear, we speculate that it represents a basolateral membrane Na+-HCO3- cotransporter or a Na+-dependent anion exchanger, which could account for transepithelial HCO3- secretion.




This article has been cited by other articles:


Home page
Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
C. S. Rogers, W. M. Abraham, K. A. Brogden, J. F. Engelhardt, J. T. Fisher, P. B. McCray Jr., G. McLennan, D. K. Meyerholz, E. Namati, L. S. Ostedgaard, et al.
The porcine lung as a potential model for cystic fibrosis
Am J Physiol Lung Cell Mol Physiol, August 1, 2008; 295(2): L240 - L263.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
A. S. Verkman
From the farm to the lab: the pig as a new model of cystic fibrosis lung disease
Am J Physiol Lung Cell Mol Physiol, August 1, 2008; 295(2): L238 - L239.
[Full Text] [PDF]


Home page
J. Physiol.Home page
J. P. Ianowski, J. Y. Choi, J. J. Wine, and J. W. Hanrahan
Mucus secretion by single tracheal submucosal glands from normal and cystic fibrosis transmembrane conductance regulator knockout mice
J. Physiol., April 1, 2007; 580(1): 301 - 314.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Respir. Cell Mol. Bio.Home page
X. Liu, M. Luo, L. Zhang, W. Ding, Z. Yan, and J. F. Engelhardt
Bioelectric Properties of Chloride Channels in Human, Pig, Ferret, and Mouse Airway Epithelia
Am. J. Respir. Cell Mol. Biol., March 1, 2007; 36(3): 313 - 323.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 2005 by the American Physiological Society.