Abstract | BACKGROUND AND PURPOSE: EXPERIMENTAL APPROACH: KEY RESULTS: In normal animals, JWH015 and JWH133 caused a concentration-dependent increase in synovial blood flow which in the case of JWH133 was blocked by the selective CB2 receptor antagonist AM630 as well as the transient receptor potential vanilloid-1 (TRPV1) antagonist SB366791. The vasodilator effect of JWH133 was significantly attenuated in both acute and chronically inflamed knees. Given alone, AM630 had no effect on joint blood flow. CONCLUSION AND IMPLICATIONS: In normal joints, the cannabinomimetic JWH133 causes hyperaemia via a CB2 and TRPV1 receptor mechanism. During acute and chronic inflammation, however, this vasodilatatory response is significantly attenuated.
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Authors | J J McDougall, V Yu, J Thomson |
Journal | British journal of pharmacology
(Br J Pharmacol)
Vol. 153
Issue 2
Pg. 358-66
(Jan 2008)
ISSN: 0007-1188 [Print] England |
PMID | 17982474
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Cannabinoids
- Receptor, Cannabinoid, CB2
- TRPV Cation Channels
- Trpv1 protein, rat
- Vasodilator Agents
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Topics |
- Administration, Topical
- Animals
- Arthritis, Experimental
(physiopathology)
- Blood Pressure
(drug effects)
- Cannabinoids
(administration & dosage, pharmacology)
- Dose-Response Relationship, Drug
- Edema
(drug therapy, pathology)
- Image Processing, Computer-Assisted
- Joints
(blood supply, drug effects)
- Male
- Rats
- Rats, Wistar
- Receptor, Cannabinoid, CB2
(drug effects)
- Regional Blood Flow
(drug effects)
- TRPV Cation Channels
(genetics)
- Vasodilator Agents
(pharmacology)
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