AJP - Lung Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Lung Cell Mol Physiol 275: L1006-L1012, 1998;
1040-0605/98 $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 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 Szarek, J. L.
Right arrow Articles by Lemke, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Szarek, J. L.
Right arrow Articles by Lemke, S.
Vol. 275, Issue 5, L1006-L1012, November 1998

Substance P and capsaicin release prostaglandin E2 from rat intrapulmonary bronchi

John L. Szarek, Beverly Spurlock, Carl A. Gruetter, and Sally Lemke

Department of Pharmacology, Marshall University School of Medicine, Huntington, West Virginia 25704-9388

We hypothesized that substance P and capsaicin would cause the release of prostaglandin E2 (PGE2) from intrapulmonary bronchi isolated from Sprague-Dawley rats. Substance P (1 µM) caused the release of PGE2, measured with enzyme immunoassay, from the isolated airway segments; PGE2 release was inhibited by the neurokinin (NK)1-receptor antagonist, RP-67580, by inhibition of cyclooxygenase with meclofenamate, and by removal of the epithelium. The release of PGE2 caused by capsaicin (1 µM) was similar in magnitude to that caused by substance P. The capsaicin-induced release of PGE2 was inhibited by desensitization of sensory nerves with capsaicin and by RP-67580, meclofenamate, and epithelial denudation. We conclude that activation of NK1 receptors on epithelium causes release of PGE2, which most likely represents the ultimate mediator of airway smooth muscle relaxation, produced by exogenous neuropeptides and by activation of the sensory nerve inhibitory system. Epithelial damage, such as that seen in asthmatic airways, would disrupt this protective system in the lungs, which could contribute to the development of airway disease.

neurokinin type 1 receptors; epithelium; C fibers


This article has been cited by other articles:


Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
J. Q. Liu, D. Yang, and R. J. Folz
A novel bronchial ring bioassay for the evaluation of small airway smooth muscle function in mice
Am J Physiol Lung Cell Mol Physiol, August 1, 2006; 291(2): L281 - L288.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
D. R. Bergren
Prostaglandin involvement in lung C-fiber activation by substance P in guinea pigs
J Appl Physiol, June 1, 2006; 100(6): 1918 - 1927.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
C. N. Fortner, J. N. Lorenz, and R. J. Paul
Chloride channel function is linked to epithelium-dependent airway relaxation
Am J Physiol Lung Cell Mol Physiol, February 1, 2001; 280(2): L334 - L341.
[Abstract] [Full Text] [PDF]


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