AJP - Lung Watch the video to learn how APS reaches out to developing nations.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Lung Cell Mol Physiol 281: L1173-L1179, 2001;
1040-0605/01 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
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 ISI Web of Science (7)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Brady, K. G.
Right arrow Articles by Drumm, M. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Brady, K. G.
Right arrow Articles by Drumm, M. L.
Vol. 281, Issue 5, L1173-L1179, November 2001

Examining basal chloride transport using the nasal potential difference response in a murine model

Kristine G. Brady1, Thomas J. Kelley2, and Mitchell L. Drumm1,2

1 Center for Human Genetics, Department of Genetics, and 2 Department of Pediatrics, Case Western Reserve University, Cleveland, Ohio 44106-4948

Epithelia of humans and mice with cystic fibrosis are unable to secrete chloride in response to a chloride gradient or to cAMP-elevating agents. Bioelectrical properties measured using the nasal transepithelial potential difference (TEPD) assay are believed to reflect these cystic fibrosis transmembrane conductance regulator (CFTR)-dependent chloride transport defects. Although the response to forskolin is CFTR mediated, the mechanisms responsible for the response to a chloride gradient are unknown. TEPD measurements performed on inbred mice were used to compare the responses to low chloride and forskolin in vivo. Both responses show little correlation between or within inbred strains of mice, suggesting they are mediated through partially distinct mechanisms. In addition, these responses were assayed in the presence of several chloride channel inhibitors, including DIDS, diphenylamine-2-carboxylate, glibenclamide, and 5-nitro-2-(3-phenylpropylamino)-benzoic acid, and a protein kinase A inhibitor, the Rp diastereomer of adenosine 3',5'-cyclic monophosphothioate (Rp-cAMPS). The responses to low chloride and forskolin demonstrate significantly different pharmacological profiles to both DIDS and Rp-cAMPS, indicating that channels in addition to CFTR contribute to the low chloride response.

cystic fibrosis; cystic fibrosis transmembrane conductance regulator; ion channel inhibitors; protein kinase A


This article has been cited by other articles:


Home page
 Am. J. Respir. Crit. Care Med.Home page
B. Lubamba, H. Lecourt, J. Lebacq, P. Lebecque, H. De Jonge, P. Wallemacq, and T. Leal
Preclinical Evidence that Sildenafil and Vardenafil Activate Chloride Transport in Cystic Fibrosis
Am. J. Respir. Crit. Care Med., March 1, 2008; 177(5): 506 - 515.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
D. B. Salinas, N. Pedemonte, C. Muanprasat, W. F. Finkbeiner, D. W. Nielson, and A. S. Verkman
CFTR involvement in nasal potential differences in mice and pigs studied using a thiazolidinone CFTR inhibitor
Am J Physiol Lung Cell Mol Physiol, November 1, 2004; 287(5): L936 - L943.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
A. M. van Heeckeren, M. D. Schluchter, M. L. Drumm, and P. B. Davis
Role of Cftr genotype in the response to chronic Pseudomonas aeruginosa lung infection in mice
Am J Physiol Lung Cell Mol Physiol, November 1, 2004; 287(5): L944 - L952.
[Abstract] [Full Text] [PDF]

Home page
 ScienceHome page
M. E. Egan, M. Pearson, S. A. Weiner, V. Rajendran, D. Rubin, J. Glockner-Pagel, S. Canny, K. Du, G. L. Lukacs, and M. J. Caplan
Curcumin, a Major Constituent of Turmeric, Corrects Cystic Fibrosis Defects
Science, April 23, 2004; 304(5670): 600 - 602.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online