Involvement of B<sub>1</sub> and B<sub>2</sub> receptors in bradykinin‐induced rat paw oedema

Campos, Maria M.; Calixto, João B.

doi:10.1111/j.1476-5381.1995.tb13305.x

Cited by 114 publications

(77 citation statements)

References 44 publications

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“…One possible explanation for these apparent contradictory results could be that the activation of B 2 Rs was having two major effects in the system-an effect on tissue cells inducing the expression B 1 Rs and a protective effect. As for the former effect, there is evidence to suggest that B 2 R activation takes place at the beginning of the inflammatory process, and that via autoregulatory mechanisms, the desensitization of B 2 Rs occurs, followed by the up-regulations of B 1 Rs (23,44). In our experiments, blockade of B 2 Rs with HOE 140 prevented the up-regulation of B 1 Rs in the intestine and lungs of reperfused animals.…”

Section: Discussionmentioning

confidence: 54%

Role of Bradykinin B2 and B1 Receptors in the Local, Remote, and Systemic Inflammatory Responses That Follow Intestinal Ischemia and Reperfusion Injury

Souza¹,

Lomez

Pinho³

et al. 2004

The Journal of Immunology

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The administration of bradykinin may attenuate ischemia and reperfusion (I/R) injury by acting on B2Rs. Blockade of B2R has also been shown to ameliorate lesions associated with I/R injury. In an attempt to explain these contradictory results, the objective of the present work was to investigate the role of and interaction between B1 and B2 receptors in a model of intestinal I/R injury in mice. The bradykinin B2R antagonist (HOE 140) inhibited reperfusion-induced inflammatory tissue injury and delayed lethality. After I/R, there was an increase in the expression of B1R mRNA that was prevented by HOE 140. In mice that were deficient in B1Rs (B1R−/− mice), inflammatory tissue injury was abrogated, and lethality was delayed and partially prevented. Pretreatment with HOE 140 reversed the protective anti-inflammatory and antilethality effects provided by the B1R−/− phenotype. Thus, B2Rs are a major driving force for B1R activation and consequent induction of inflammatory injury and lethality. In contrast, activation of B2Rs may prevent exacerbated tissue injury and lethality, an effect unmasked in B1R−/− mice and likely dependent on the vasodilatory actions of B2Rs. Blockade of B1Rs could be a more effective strategy than B2 or B1/B2 receptor blockade for the treatment of the inflammatory injuries that follow I/R.

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Section: Discussionmentioning

confidence: 54%

Role of Bradykinin B2 and B1 Receptors in the Local, Remote, and Systemic Inflammatory Responses That Follow Intestinal Ischemia and Reperfusion Injury

Souza¹,

Lomez

Pinho³

et al. 2004

The Journal of Immunology

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“…The contralateral paw received 0.1 mL PBS and was used as a control. Oedema was measured by the use of a plethysmometer (Ugo Basile) at several time points (0.5, 1, 2 and 4 h for Cg and 10, 20, 30, 60 and 120 min for BK) following the injection of inflammatory mediators as described previously (Campos and Calixto, 1995;Campos et al, 1996). Oedema is expressed in mL as the difference between the test and control paws.…”

Section: Methodsmentioning

confidence: 99%

Phytochemical and antioedematogenic studies of commercial copaiba oils available in Brazil

Veiga

Zunino

Calixto

et al. 2001

Phytotherapy Research

103

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The composition of eight samples of commercial copaiba oils, used in the Amazonian region as antiinflammatory agents and available in popular markets, were analysed by gas chromatography/mass spectrometry (HRGC-MS). Major differences were observed in their chemical composition and some adulterations were pointed out. When tested in vivo oils 1 and 3, and to a lesser extent oil 6, significantly inhibited bradykinin-induced oedema formation. The other tested oils had no effect. When assessed in carrageenan-induced oedema formation, oils 1, 2 and 6, but not oil 3, significantly attenuated the oedema formation. The other tested oils failed to affect carrageenan-induced paw oedema. Oils 1 and 6 were further fractionated and several sesquiterpenes and diterpenes were detected. It is suggested that the naturally occurring sesquiterpenes present in the copaiba oils seem to be responsible for the antiinflammatory action reported in the folk medicine. Furthermore, our results clearly show an adulteration in copaiba oils available in Brazil.

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“…The experiments were conducted according to the procedures described previously (34). The animals received a 0.1 ml intradermal (i.d.)…”

Section: Measurement Of Rat Paw Edemamentioning

confidence: 99%

Kinin B1 Receptor Up-Regulation after Lipopolysaccharide Administration: Role of Proinflammatory Cytokines and Neutrophil Influx

Passos

Fernandes

Campos

et al. 2004

The Journal of Immunology

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Several studies have now clearly established the ability of LPS to induce bradykinin B1 receptor up-regulation in vivo and the functional relevance of this up-regulation for the pathophysiological effects of LPS. Using an in vivo system in which LPS is injected locally into the rat paw, we have examined the potential contribution of proinflammatory cytokines, NF-κB activation, and neutrophil influx for the functional and molecular up-regulation of the bradykinin B1 receptor. Treatment with LPS resulted in a rapid and sustained functional up-regulation of B1 receptors in the rat paw that correlated with the increase in B1 receptor mRNA levels. B1 receptor up-regulation is preceded by the rapid activation of the transcription factor NF-κB and the production of proinflammatory cytokines, including TNF-α and IL-1β. More importantly, blockade of NF-κB translocation, TNF-α, or IL-1β prevented the functional and molecular up-regulation of B1 receptors. Injection of LPS also induced the influx of neutrophils that followed the peak of cytokine production and associated with the persistent activation of NF-κB and functional B1 receptor up-regulation. Blockade of neutrophil influx with platelet-activating factor receptor antagonists or cell adhesion molecule blockers prevented B1 receptor up-regulation. Thus, by acting in cooperation and in a coordinated, timely manner, TNF-α, IL-1β, neutrophils, and the transcription factor NF-κB are major and essential players in the ability of LPS to induce B1 receptor expression in vivo.

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Involvement of B₁ and B₂ receptors in bradykinin‐induced rat paw oedema

Cited by 114 publications

References 44 publications

Role of Bradykinin B2 and B1 Receptors in the Local, Remote, and Systemic Inflammatory Responses That Follow Intestinal Ischemia and Reperfusion Injury

Role of Bradykinin B2 and B1 Receptors in the Local, Remote, and Systemic Inflammatory Responses That Follow Intestinal Ischemia and Reperfusion Injury

Phytochemical and antioedematogenic studies of commercial copaiba oils available in Brazil

Kinin B1 Receptor Up-Regulation after Lipopolysaccharide Administration: Role of Proinflammatory Cytokines and Neutrophil Influx

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Involvement of B1 and B2 receptors in bradykinin‐induced rat paw oedema

Cited by 114 publications

References 44 publications

Role of Bradykinin B2 and B1 Receptors in the Local, Remote, and Systemic Inflammatory Responses That Follow Intestinal Ischemia and Reperfusion Injury

Role of Bradykinin B2 and B1 Receptors in the Local, Remote, and Systemic Inflammatory Responses That Follow Intestinal Ischemia and Reperfusion Injury

Phytochemical and antioedematogenic studies of commercial copaiba oils available in Brazil

Kinin B1 Receptor Up-Regulation after Lipopolysaccharide Administration: Role of Proinflammatory Cytokines and Neutrophil Influx

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Involvement of B₁ and B₂ receptors in bradykinin‐induced rat paw oedema