ArticleBritish journal of pharmacology2005
The role of joint nerves and mast cells in the alteration of vasoactive intestinal peptide (VIP) sensitivity during inflammation progression in rats.
Article in British journal of pharmacology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 22 citations in OpenAlex.
- Neuro-immune interactions in urticaria:a pruritus-centric dissection.Frontiers in immunology · 2026Review
- Cannabinoid control of neurogenic inflammation.British journal of pharmacology · 2020Review
- Role of vasoactive intestinal peptide in osteoarthritis.Journal of biomedical science · 2016Review
- Mechanisms and Mediators That Drive Arthritis Pain.Current osteoporosis reports · 2015Review
- Agonistic behavior of PACAP6-38 on sensory nerve terminals and cytotrophoblast cells.Journal of molecular neuroscience : MN · 2008Article
- The symptoms of osteoarthritis and the genesis of pain.Rheumatic diseases clinics of North America · 2008Review
- In vivo effects of CB2 receptor-selective cannabinoids on the vasculature of normal and arthritic rat knee joints.British journal of pharmacology · 2008Article
- Stimulation of sensory neuropeptide release by nociceptin/orphanin FQ leads to hyperaemia in acutely inflamed rat knees.British journal of pharmacology · 2006Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study examined the peripheral effects of vasoactive intestinal peptide (VIP) on rat knee joint blood flow during acute and chronic inflammation. The involvement of joint nerves and synovial mast cells on these effects was also investigated. Prior to blood flow assessment, animals were deeply anaesthetised with ethyl carbamate (urethane; 2 mg kg(-1) i.p.). Local application of VIP (10(-13)-10(-9) mol) onto the capsular surface of normal rat knee joints caused a dose-dependent increase in synovial perfusion with an ED50 of 1.2 x 10(-11) mol. The dilator effect of the peptide was transient with the maximal response occurring approximately 1 min after drug administration. VIP-induced vasodilatation was blocked by co-administration of the VIP receptor antagonist VIP(6-28) (10(-9) mol). The inhibitory effect of the antagonist was consistent across the entire VIP dose range (P=0.01). The vasoresponsiveness to VIP was significantly attenuated in acutely inflamed joints; however, surgical denervation of acutely inflamed knees re-established the vasodilator effect of the neuropeptide. Topical application of VIP to 1- and 3-week adjuvant monoarthritic knees produced a hyperaemic response, which was not significantly different from normal (P=0.06 and 0.73 for 1- and 3-week adjuvant treated joints, respectively). Stabilisation of synovial mast cells by disodium cromoglycate (cromolyn) pretreatment did not alter the vasoresponsiveness to VIP in acute or chronically inflamed joints. The vasodilatatory effect of VIP is lost during acute knee joint inflammation and this abrogated effect is neurally dependent. In the chronic phase of knee joint inflammation, VIP-mediated hyperaemia recovers to normal levels. Synovial mast cells do not influence the vasomotor effects of exogenously applied VIP in inflamed knee joints.
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