An examination of neurogenic mechanisms involved in mustard oil-induced inflammation in the mouse

A D Grant, E Pinter, A M L Salmon, S D Brain

Research output: Contribution to journalArticlepeer-review

43 Citations (Scopus)

Abstract

The mechanisms by which topical mustard oil causes vasodilatation in the mouse were investigated using the tachykinin NK1 receptor antagonist SR140333 and the calcitonin gene-related peptide (CGRP) antagonist BIBN4096BS. alongside alphaCGRP or NK1 receptor knockout mice. Blood flow was assessed by laser Doppler flowmetry and plasma extravasation by I-125-albumin accumulation. Mustard oil produced significant plasma extravasation and vasodilatation in wild type mice. although the plasma extravasation was less than that seen with capsaicin whilst the vasodilatation was greater. The plasma extravasation was abolished in tachykinin NK1 knockout mice. whilst the vasodilatation was enhanced. BIBN4096BS was unable to inhibit the vasodilatation in wild type mice but abolished it in the NK1 knockout mice. In alphaCGRP knockout mice, mustard oil also caused plasma extravasation and vasodilatation. which were both inhibited by treatment with SR140333. These data suggest that both a tachykinin NK1 receptor agonist and a CGRP agonist are active as vasodilators, producing redundancy, requiring blockade of both mediators to prevent vasodilatation. (C) 2004 Elsevier B.V. All rights reserved.
Original languageEnglish
Pages (from-to)273 - 280
Number of pages8
JournalEuropean Journal of Pharmacology
Volume507
Issue number1-3
DOIs
Publication statusPublished - 10 Jan 2005

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