| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Articles in PresS, published online ahead of print April 12, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00277.2001
Submitted on July 23, 2001
Accepted on April 4, 2002
1 Physiology, University of South Alabama, Mobile, AL, USA
2 Child Health, University of Dundee, Dundee, Scotland, United Kingdom
* To whom correspondence should be addressed. E-mail: sballard{at}usamail.usouthal.edu.
Because of its possible importance in cystic fibrosis (CF) pulmonary pathogenesis, the effect of anion and liquid secretion inhibitors on airway mucociliary transport was examined. When excised porcine tracheas were treated with ACh to induce gland liquid secretion, the rate of mucociliary transport was increased nearly three-fold from 2.5±0.5 mm/min to 6.8±0.8 mm/min. Pretreatment with both bumetanide and dimethylamiloride (DMA), to respectively inhibit Cl- and HCO3- secretion, significantly reduced mucociliary transport in the presence of ACh by 92%. Pretreatment with the anion channel blocker NPPB similarly reduced mucociliary transport in ACh-treated airways by 97%. These agents did not, however, reduce ciliary beat frequency. Luminal application of benzamil to block liquid absorption significantly reversed the inhibitory effects of bumetanide and DMA on mucociliary transport. We conclude that anion and liquid secretion is essential for normal mucociliary transport in glandular airways. Since the CFTR likely mediates Cl-, HCO3-, and liquid secretion in normal glands, we speculate that impairment of gland liquid secretion significantly contributes to defective mucociliary transport in CF.
This article has been cited by other articles:
|
|
 |
|
  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]
|
|
|
|
 |
|
 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]
|
|
|
|
|
|
B. R. Grubb, J. H. Jones, and R. C. Boucher Mucociliary transport determined by in vivo microdialysis in the airways of normal and CF mice Am J Physiol Lung Cell Mol Physiol, March 1, 2004; 286(3): L588 - L595. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. J. Thornton and J. K. Sheehan From Mucins to Mucus: Toward a More Coherent Understanding of This Essential Barrier Proceedings of the ATS, January 1, 2004; 1(1): 54 - 61. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. R. Cobb, L. Fan, T. E. Kovacs, E. J. Sorscher, and J. P. Clancy Adenosine Receptors and Phosphodiesterase Inhibitors Stimulate Cl- Secretion in Calu-3 Cells Am. J. Respir. Cell Mol. Biol., September 1, 2003; 29(3): 410 - 418. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
