JOURNAL HOME CME HOME THIS MONTH PAST ISSUES ETOC COLLECTIONS
AUTHORS REVIEWERS EDITORIAL BOARD FEEDBACK RSS HELP
A&A International Anesthesia Research Society
QUICK SEARCH:   [advanced]


     

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
Services
Right arrow Email this article to a colleague
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 (5)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Klass, M.
Right arrow Articles by Csete, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Klass, M.
Right arrow Articles by Csete, M.
Related Collections
Right arrow Mechanisms
Right arrow Pain
Right arrow Pharmacology

Anesth Analg 2005;101:1757-1762
© 2005 International Anesthesia Research Society
doi: 10.1213/01.ANE.0000180766.74782.7E

PAIN MEDICINE

A Role for Endothelin in Neuropathic Pain After Chronic Constriction Injury of the Sciatic Nerve

Markus Klass, MD, PhD, Allen Hord, MD, Melissa Wilcox, BA, Don Denson, PhD, and Marie Csete, MD, PhD

Departments of Anesthesiology and Cell Biology, Emory University School of Medicine, Atlanta, Georgia

Address correspondence and reprint requests to Marie Csete MD, PhD, Emory Anesthesiology Laboratories, 1462 Clifton Rd NE, Room 420, Atlanta GA 30322. Address e-mail to marie.csete{at}emoryhealthcare.org.

The purpose of this study was to explore the role of endothelin in neuropathic pain. Endothelins (ET) are a family (ET-1, ET-2, ET-3) of ubiquitously expressed peptides involved in control of vascular tone. Injected ET-1 causes intense pain via activation of ETA receptors, modulated by analgesic signals initiated by ETB receptor activation. Using a rat model of chronic constriction injury of the sciatic nerve, we found that pharmacologic ETA receptor antagonism acutely and significantly reduced thermal and mechanical hyperalgesic responses 5 days after injury. Furthermore, ET-1 and the ETA receptor are locally upregulated at the site of chronic constriction injury at both the message and the protein levels, suggesting that ET-1 may be involved in establishing pain after the injury. These data point to ET-1 as an important mediator of pain in general and suggest that ETA antagonism deserves study as a potential novel therapy for neuropathic pain.




This article has been cited by other articles:


Home page
 Anesth. Analg.Home page
M. Klass, V. Gavrikov, D. Drury, B. Stewart, S. Hunter, D. D. Denson, A. Hord, and M. Csete
Intravenous Mononuclear Marrow Cells Reverse Neuropathic Pain from Experimental Mononeuropathy
Anesth. Analg., April 1, 2007; 104(4): 944 - 948.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
U. C. Kopp, M. Z. Cicha, and L. A. Smith
Differential effects of endothelin on activation of renal mechanosensory nerves: stimulatory in high-sodium diet and inhibitory in low-sodium diet
Am J Physiol Regulatory Integrative Comp Physiol, November 1, 2006; 291(5): R1545 - R1556.
[Abstract] [Full Text] [PDF]


Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press
Copyright © 2005 by the International Anesthesia Research Society.