ArticleBritish journal of pharmacology2012
Inflammatory muscle pain is dependent on the activation of kinin B₁ and B₂ receptors and intracellular kinase pathways.
Article in British journal of pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- STIM1 functionally couples to transient receptor potential ankyrin 1 contributing to nociception.Pain · 2025Article
- The intersection of endocrine signaling and neuroimmune communication regulates muscle inflammation-induced nociception in neonatal mice.Brain, behavior, and immunity · 2025Article
- TRPV4 Activation and its Intracellular Modulation Mediated by Kinin Receptors Contribute to Painful Symptoms Induced by Anastrozole.Molecular neurobiology · 2024Article
- Effect of curcumin on formalin-induced muscle pain in male rats: role of local cyclooxygenase system.Veterinary research forum : an international quarterly journal · 2024Article
- Kinins: Locally formed peptides during inflammation with potential use in tissue regeneration.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Kinin BPharmaceutics · 2023Article
- Bradykinin receptor expression and bradykinin-mediated sensitization of human sensory neurons.bioRxiv : the preprint server for biology · 2023Article
- Kinin BPharmaceutics · 2023Article
- Involvement of bradykinin and bradykinin B1 receptor in patients with endometriosis.Experimental and therapeutic medicine · 2021Article
- The kinin BInflammopharmacology · 2019Article
- Angiotensin-Converting Enzyme Related-Polymorphisms on Inflammation, Muscle and Myocardial Damage After a Marathon Race.Frontiers in genetics · 2019Article
- Oxidative Stress Contributes to Fracture/Cast-Induced Inflammation and Pain in a Rat Model of Complex Regional Pain Syndrome.The journal of pain · 2018Article
- Kinin Receptors Sensitize TRPV4 Channel and Induce Mechanical Hyperalgesia: Relevance to Paclitaxel-Induced Peripheral Neuropathy in Mice.Molecular neurobiology · 2018Article
- Preconditioning Contractions Suppress Muscle Pain Markers after Damaging Eccentric Contractions.Pain research & management · 2018Article
- Review
- A Role for Bradykinin Signaling in Chronic Vulvar Pain.The journal of pain · 2016Article
- Article
- Recurrent Bilateral Focal Myositis.Internal medicine (Tokyo, Japan)Article
- Anatomical and physiological factors contributing to chronic muscle pain.Current topics in behavioral neurosciencesArticle
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeB(1) and B(2) kinin receptors are involved in pain transmission but they may have different roles in the muscle pain induced by intense exercise or inflammation. We investigated the contribution of each of these receptors, and the intracellular pathways involved, in the initial development and maintenance of the muscle pain associated with inflammation-induced tissue damage. EXPERIMENTAL APPROACH: Mechanical hyperalgesia was measured using the Randall-Selitto apparatus after injecting 5% formalin solution into the gastrocnemius muscle in mice treated with selective antagonists for B(1) or B(2) receptors. The expression of kinin receptors and cytokines and the activation of intracellular kinases were monitored by real-time PCR and immunohistochemistry. KEY
resultsThe i.m. injection of formalin induced an overexpression of B(1) and B(2) receptors. This overexpression was associated with the mechanical hyperalgesia induced by formalin because treatment with B(1) receptor antagonists (des-Arg(9) [Leu(8)]-BK, DALBK, and SSR240612) or B(2) receptor antagonists (HOE 140 and FR173657) prevented the hyperalgesia. Formalin increased myeloperoxidase activity, and up-regulated TNF-α, IL-1β and IL-6 in gastrocnemius. Myeloperoxidase activity and TNF-α mRNA expression were inhibited by either DALBK or HOE 140, whereas IL-6 was inhibited only by HOE 140. The hyperalgesia induced by i.m. formalin was dependent on the activation of intracellular MAPKs p38, JNK and PKC. CONCLUSIONS AND IMPLICATIONS: Inflammatory muscle pain involves a cascade of events that is dependent on the activation of PKC, p38 and JNK, and the synthesis of IL-1β, TNF-α and IL-6 associated with the up-regulation of both B(1) and B(2) kinin receptors.
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