The role of kinin B1 receptors in the nociception produced by peripheral protein kinase C activation in mice

Ferreira, Juliano; Trichês, Karen M.; Medeiros, Rodrigo; Cabrini, Daniela Almeida; Mori, Marcelo A.S.; Pesquero, João Bosco; Bäder, Michael; Calixto, João B.

doi:10.1016/j.neuropharm.2007.11.008

Cited by 32 publications

(20 citation statements)

References 52 publications

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“…Our result reveals that BMD abolished bradykinininduced nociception. The action of bradykinin is mediated through the stimulation of two subtypes receptors, denoted B 1 and B 2 , and by a direct activation of PKC-and an indirect activation of the PKA-signaling pathways (Campos et al, 2006;Ferreira et al, 2008). Several studies have also demonstrated the peripheral involvement of PK A and C in a number of persistent pain models (Cunha et al, 1999(Cunha et al, , 2004Joseph & Levine, 2003;Souza et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Antinociceptive and anti-hyperalgesic effects of bis(4-methylbenzoyl) diselenide in mice: Evidence for the mechanism of action

Donato

Pavin

Goes

et al. 2014

Pharmaceutical Biology

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(2015) Antinociceptive and anti-hyperalgesic effects of bis(4-methylbenzoyl) diselenide in mice: Evidence for the mechanism of action, Pharmaceutical Biology, 53:3, 395-403, DOI: 10.3109/13880209.2014 -nitro-L-arginine ( L-NOARG), but the effect of BMD was not abolished by naloxone. Mechanical hyperalgesia induced by Cg and CFA was attenuated by BMD, 70 ± 4% and 65 ± 4%, respectively. Furthermore, a single oral dose of BMD did not change plasma aspartate (AST) and alanine aminotransferase (ALT) activities or urea and creatinine levels. Conclusion: BMD demonstrated as a promising compound because of the antinociceptive and anti-hyperalgesic properties in mice.

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Section: Discussionmentioning

confidence: 99%

Antinociceptive and anti-hyperalgesic effects of bis(4-methylbenzoyl) diselenide in mice: Evidence for the mechanism of action

Donato

Pavin

Goes

et al. 2014

Pharmaceutical Biology

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“…Our results also indicated that the intracellular second messenger PKC exerts a relevant role in mediating the hyperalgesia induced by formalin in muscle pain. Within the PKC family, the PKCε isoform has been reported to have a particular contribution towards nociception and it can act as a second messenger in the activation of kinin receptors (Cesare et al ., 1999; Ferreira et al ., 2005; 2008). Furthermore, PKCε is only involved in inflammatory muscle pain (Dina et al ., 2008b).…”

Section: Discussionmentioning

confidence: 99%

Inflammatory muscle pain is dependent on the activation of kinin B₁ and B₂ receptors and intracellular kinase pathways

Meotti

Campos

Silva

et al. 2012

British J Pharmacology

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BACKGROUND AND PURPOSEB1 and B2 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 APPROACHMechanical hyperalgesia was measured using the Randall-Selitto apparatus after injecting 5% formalin solution into the gastrocnemius muscle in mice treated with selective antagonists for B1 or B2 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 B1 and B2 receptors. This overexpression was associated with the mechanical hyperalgesia induced by formalin because treatment with B1 receptor antagonists (des-Arg 9 [Leu 8 ]-BK, DALBK, and SSR240612) or B2 receptor antagonists (HOE 140 and FR173657) prevented the hyperalgesia. Formalin increased myeloperoxidase activity, and up-regulated TNF-a, IL-1b and IL-6 in gastrocnemius. Myeloperoxidase activity and TNF-a 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 IMPLICATIONSInflammatory muscle pain involves a cascade of events that is dependent on the activation of PKC, p38 and JNK, and the synthesis of IL-1b, TNF-a and IL-6 associated with the up-regulation of both B1 and B2 kinin receptors.Abbreviations DALBK,

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“…Kinins release a large number of inflammatory mediators such as prostaglandins, nitric oxide and neuropeptides such as neurokinins, which in turn amplify the nociceptive responses [32]. Bradykinin which primarily acts at B 2 kinin receptors is one of the most potent endogenous pain inducing substances, and its role in the nociceptive process has been extensively reviewed [33]. Bradykinin is found to sensitize primary afferent neurons through interactions with most inflammatory mediators, including prostaglandins and cytokines, and through the release of histamine from mast cells which will lead to hyperalgesia.…”

Section: Discussionmentioning

confidence: 99%

Zerumbone-Induced Antinociception: Involvement of the l-Arginine-Nitric Oxide-cGMP -PKC-K+ATP Channel Pathways

Perimal

Akhtar

Mohamad

et al. 2010

Basic &Amp; Clinical Pharmacology &Amp; Toxicology

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This study investigated the antinociceptive effects of zerumbone in chemical behavioural models of nociception in mice. Zerumbone given through intraperitoneal route (i.p.) produced dose-related antinociception when assessed on acetic acid-induced abdominal writhing test in mice. In addition, the i.p. administration of zerumbone exhibited significant inhibition of the neurogenic pain induced by intraplantar (i.pl.) injection of capsaicin and bradykinin. Likewise, zerumbone given by i.p. route reduced the nociception produced by i.pl. injection of glutamate and phorbol myristate acetate (PMA). The antinociception caused by zerumbone in the acetic acid test was significantly attenuated by i.p. pre-treatment of mice with L-arginine (nitric oxide precursor) and glibenclamide (ATP-sensitive K + channel inhibitor). However, the antinociception of zerumbone was enhanced by methylene blue (non-specific gyanylyl cyclase inhibitor). Together, these results indicate that zerumbone produces pronounced antinociception against chemical models of nociception in mice. It also strongly suggests that the L-arginine-nitric oxide-cGMP-PKC-K + ATP channel pathways, the TRPV1 and kinin B2 receptors play an important role in the zerumbone-induced antinociception.

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The role of kinin B1 receptors in the nociception produced by peripheral protein kinase C activation in mice

Cited by 32 publications

References 52 publications

Antinociceptive and anti-hyperalgesic effects of bis(4-methylbenzoyl) diselenide in mice: Evidence for the mechanism of action

Antinociceptive and anti-hyperalgesic effects of bis(4-methylbenzoyl) diselenide in mice: Evidence for the mechanism of action

Inflammatory muscle pain is dependent on the activation of kinin B₁ and B₂ receptors and intracellular kinase pathways

Zerumbone-Induced Antinociception: Involvement of the l-Arginine-Nitric Oxide-cGMP -PKC-K+ATP Channel Pathways

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The role of kinin B1 receptors in the nociception produced by peripheral protein kinase C activation in mice

Cited by 32 publications

References 52 publications

Antinociceptive and anti-hyperalgesic effects of bis(4-methylbenzoyl) diselenide in mice: Evidence for the mechanism of action

Antinociceptive and anti-hyperalgesic effects of bis(4-methylbenzoyl) diselenide in mice: Evidence for the mechanism of action

Inflammatory muscle pain is dependent on the activation of kinin B1 and B2 receptors and intracellular kinase pathways

Zerumbone-Induced Antinociception: Involvement of the l-Arginine-Nitric Oxide-cGMP -PKC-K+ATP Channel Pathways

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Inflammatory muscle pain is dependent on the activation of kinin B₁ and B₂ receptors and intracellular kinase pathways