ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]1995
Involvement of substance P as a mediator in capsaicin-induced mouse ear oedema.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 36 citations in OpenAlex.
- An updated review on molecular mechanisms underlying the anticancer effects of capsaicin.Food science and biotechnology · 2017Review
- Neurogenic inflammation after traumatic brain injury and its potentiation of classical inflammation.Journal of neuroinflammation · 2016Review
- Cecropia pachystachya: a species with expressive in vivo topical anti-inflammatory and in vitro antioxidant effects.BioMed research international · 2014Article
- Role of substance P in renal injury during DOCA-salt hypertension.Endocrinology · 2012Article
- Enhanced skin permeation using polyarginine modified nanostructured lipid carriers.Journal of controlled release : official journal of the Controlled Release Society · 2012Article
- Effect of oleic acid modified polymeric bilayered nanoparticles on percutaneous delivery of spantide II and ketoprofen.Journal of controlled release : official journal of the Controlled Release Society · 2012Article
- Skin permeating nanogel for the cutaneous co-delivery of two anti-inflammatory drugs.Biomaterials · 2012Article
- A new pharyngitis model using capsaicin in rats.General pharmacology · 1998Article
- Effect of the tachykinin receptor antagonists, SR 140333, FK 888, and SR 142801, on capsaicin-induced mouse ear oedema.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 1996Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We examined the involvement of substance P (SP) in mouse ear oedema induced by topical application of capsaicin (250 micrograms/ear). Reapplication of capsaicin at 4 h, 24 h, and 48 h after initial treatment did not induce a second oedema response. Oedema induced after the second application was significantly (p < 0.01 or p < 0.001) suppressed for up to 30 days but was observed when capsaicin was applied 40 days after initial treatment. Topical pretreatment of ears with capsaicin at 4 h, 24 h and 48 h before i.v. injection of SP (5 micrograms/kg) did not cause a significant inhibition of plasma extravasation in ear skin. NK1 receptor antagonists such as RP 67580 (ED50:0.19 mg/kg, i.v.), spantide II (ED50:0.33 mg/kg, i.v.), and GR 82334 (ED50:0.26 mg/kg, i.v.), inhibited capsaicin-induced ear oedema, whereas SR 48968 (2.0 mg/kg, i.v.), a NK2 receptor antagonist, had no effect. Furthermore, RP 67580 (0.5 kg/mg, i.v.) inhibited the oedema response induced by reapplication of capsaicin at 50 days after initial treatment. These results indicate that tachyphylaxis of capsaicin-induced oedema is reversible and suggest that this response may be due mainly to a reduction of SP in sensory neurones but not to any loss of responsiveness of NK1 receptors. We also conclude that SP and NK1 receptors are involved predominantly in the development of capsaicin-induced mouse ear oedema.
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