2000
DOI: 10.1038/sj.bjp.0703225
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Contribution of B2 receptors for bradykinin in Arthus reaction‐induced plasma extravasation in wild‐type or B2 transgenic knockout mice

Abstract: 1 The aim of the present study was to investigate the contribution of bradykinin (BK) B 1 and B 2 receptors in a model of type III hypersensitivity, the reverse passive Arthus reaction (RPA), in wildtype mice and transgenic B 2 knockout littermates. 2 BK (10 mg mouse 71 ) or bovine serum albumin (0.5 mg mouse 71 ) induced a sustained Evans blue extravasation for more than 80 min in naive or rabbit anti-bovine serum albumin-treated mice (RPA model), respectively. The response to the two stimuli was prevented by… Show more

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Cited by 15 publications
(12 citation statements)
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References 33 publications
(34 reference statements)
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“…Factor XII initiates the activation of the kinin cascade, thereby leading to bradykinin generation. Bradykinin exerts a modulatory effect on IC pneumonitis in mice, because blockade of the bradykinin B 2 receptor increases PMN infiltration but not their activation nor the hemorrhagic lesion [56] and also reduces plasma leakage [36]. The difficulty in demonstrating the activation of the coagulation cascade in IC-mediated lesions is best explained by the increased activity of the fibrinolytic system triggered by tissue-type plasminogen activator released from mast cells [57] and endothelium [58] in response to the inflammatory mediators generated under these conditions.…”
Section: Endothelium-derived Autacoidsmentioning
confidence: 99%
See 1 more Smart Citation
“…Factor XII initiates the activation of the kinin cascade, thereby leading to bradykinin generation. Bradykinin exerts a modulatory effect on IC pneumonitis in mice, because blockade of the bradykinin B 2 receptor increases PMN infiltration but not their activation nor the hemorrhagic lesion [56] and also reduces plasma leakage [36]. The difficulty in demonstrating the activation of the coagulation cascade in IC-mediated lesions is best explained by the increased activity of the fibrinolytic system triggered by tissue-type plasminogen activator released from mast cells [57] and endothelium [58] in response to the inflammatory mediators generated under these conditions.…”
Section: Endothelium-derived Autacoidsmentioning
confidence: 99%
“…Intravital fluorescence microscopy techniques have enabled the visualization of antigen slowly diffusing into the perivenular sites in naïve animals, whereas in sensitized animals, antigen leakage enables IC formation and a rapid extravasation of plasma [30] mediated by PAF [31] and other mediators released from both perivascular macrophages and mast cells upon FcgR crosslinking [32][33][34]. Both C5a anaphylatoxin [35] and bradykinin [36] contribute to plasma leakage as well. Massive influx of PMNs and hemorrhagic lesions occur after 24 hours [37], as it happens, for instance, in the lungs and skin, whereas degradation of proteoglycans is observed in joints [37].…”
Section: Pathophysiological Events Following Intravascular Formation mentioning
confidence: 99%
“…However, the role of bradykinin receptors in this type of lung inflammation was never investigated. In immune complex-induced inflammation in the peritoneal cavity, bradykinin has an important role in the mechanism of plasma extravasation and this action seems to be mediated directly by bradykinin B 2 receptors [16].…”
Section: Introductionmentioning
confidence: 99%
“…Thus, specific B 2 receptor antagonists or inactivation of the B 2 receptor in knockout mice prevent specific aspects of the inflammatory response in specific models, e.g., tissue swelling and systemic signs of inflammation in peptidoglycan-induced arthritis in the Lewis rat (Uknis et al, 2001) and plasma extravasation in the Arthus reaction (Samadfam et al, 2000). B 2 receptor antagonism may have a special interest in some forms of vasogenic edema, the brain edema that follows head trauma or stroke and hereditary angioedema.…”
Section: B Inflammationmentioning
confidence: 99%