Source:http://linkedlifedata.com/resource/pubmed/id/14670807
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
2004-3-8
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pubmed:abstractText |
Endomorphin-1 is a short-chain neuropeptide with a high affinity fo the mu-opioid receptor and has recently been localized in acutely inflamed knee joints where it was found to reduce inflammation. The present study examined the propensity of endomorphin-1 to modulate synovial blood flow in normal and adjuvant-inflamed at knee joints. Under deep urethane anesthesia, endomorphin-1 was topically applied to exposed normal and 1 wk adjuvant monoarthritic knee joints (0.1 ml bolus; 10(-12)-10(-9) mol). Relative changes in articular blood flow were measured by laser Doppler perfusion imaging and vascular resistances in response to the opioid were calculated. In normal knees, endomorphin-1 caused a dose-dependent increase in synovial vascular resistance and this effect was significantly inhibited by the specific mu-opioid receptor antagonist d-Phe-Cys-Tyr-d-Trp-O n-Thr-Pen-Th amide (CTOP) (P < 0.0001, 2-factor ANOVA, n = 5-7). One week after adjuvant inflammation, the hypoaemic effect of endomorphin-1 was completely abolished (P < 0.0001, 2-factor ANOVA, n = 5-7). Immunohistochemical analysis of normal and adjuvant-inflamed joints showed a ninefold increase in endomorphin-1 levels in the monoarthritic knee compared with normal control. Western blotting and immunohistochemistry revealed a moderate number of mu-opioid receptors in normal knees; however, mu-opioid receptors were almost undetectable in arthritic joints. These findings demonstrate that peripheral administration of endomorphin-1 reduces knee joint blood flow and this effect is not sustainable during advanced inflammation. The loss of this hypoaemic response appears to be due to down regulation of mu-opioid receptors as a consequence of endomorphin-1 accumulation within the arthritic joint.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Oligopeptides,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Opioid, mu,
http://linkedlifedata.com/resource/pubmed/chemical/Somatostatin,
http://linkedlifedata.com/resource/pubmed/chemical/endomorphin 1,
http://linkedlifedata.com/resource/pubmed/chemical/phenylalanyl-cyclo(cysteinyltyrosyl-...
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0363-6119
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
286
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
R634-41
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:14670807-Animals,
pubmed-meshheading:14670807-Arthritis, Experimental,
pubmed-meshheading:14670807-Blotting, Western,
pubmed-meshheading:14670807-Dose-Response Relationship, Drug,
pubmed-meshheading:14670807-Immunohistochemistry,
pubmed-meshheading:14670807-Joints,
pubmed-meshheading:14670807-Male,
pubmed-meshheading:14670807-Muscle, Smooth, Vascular,
pubmed-meshheading:14670807-Oligopeptides,
pubmed-meshheading:14670807-Rats,
pubmed-meshheading:14670807-Rats, Wistar,
pubmed-meshheading:14670807-Receptors, Opioid, mu,
pubmed-meshheading:14670807-Regional Blood Flow,
pubmed-meshheading:14670807-Somatostatin,
pubmed-meshheading:14670807-Vascular Resistance
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pubmed:year |
2004
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pubmed:articleTitle |
Loss of vasomotor responsiveness to the mu-opioid receptor ligand endomorphin-1 in adjuvant monoarthritic rat knee joints.
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pubmed:affiliation |
Department of Physiology & Biophysics, University of Calgary, 3330 Hospital Drive NW, Calgary, Alberta, Canada T2N 4N1. mcdougaj@ucalgary.ca
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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