B1 and B2 antagonists and bradykinin-induced blood flow in rat skin inflammation

Cao, Thong V.; Brain, Susan D.; Khodr, Bereha; Khalil, Zeinab

doi:10.1007/pl00000307

Cited by 6 publications

(3 citation statements)

References 27 publications

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“…Our experiments clearly demonstrate that BK-induced PE in the rat knee is dose-dependent, and is specifically mediated by B2 subtype receptors, but not by B1, as indicated by antagonist blockade results. These results are in agreement with previous reports using similar animal models [ 3 , 35 , 36 ]. Early studies showed that B2 receptors are expressed in human synovial tissues [ 37 ] and that BK can be released from peripheral nerve terminals, as well as from peripheral tissues and cells including endothelial cells and neutrophils, upon nociceptive stimulation [ 37 – 40 ].…”

Section: Discussionsupporting

confidence: 94%

“…The expression of B1 could, however, be upregulated over a period of hours following a chronic exposure to noxious stimuli or inflammation factors [ 41 ]. Our experimental knee perfusion model was designed to analyze acute inflammation events within 1 h. Previous studies have reported that B1 receptors can be induced and activated in chronic inflammation [ 36 ]. Another possible reason is that our present study only used BK in its full-length peptide form, which is selective for the B2 receptors and much less selective for the B1 [ 41 ].…”

Section: Discussionmentioning

confidence: 99%

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Receptor mediation and nociceptin inhibition of bradykinin-induced plasma extravasation in the knee joint of the rat

et al. 2009

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Objective and designThe aim was to investigate the signaling mechanisms and regulation of bradykinin (BK)-induced inflammation in rat knee joint.Materials and methodsKnee joints of anesthetized rats were perfused with BK (0.1–1.0 μM), and synovial plasma extravasation (PE) was evaluated by spectrophotometrical measurement of Evans Blue leakage. To examine the signaling pathway, B1 antagonist [des-Arg10]-HOE140 (0.1–1.0 μM) and B2 antagonist HOE140 (0.05–1.0 μM), calcitonin gene-related peptide (CGRP) antagonist CGRP8-37 (0.5–1.0 μM), prostaglandin E2 antagonist AH-6809 (0.1–1.0 μM), and histamine H1 antagonist mepyramine (0.1–1.0 μM) were used. Nociceptin (0.0001–1.0 μM) and antagonist J-113397 were tested for modulation of BK-induced PE. The analyses were compared side-by-side with 5-hydroxytryptamine-induced PE.ResultsBK perfusion dose-dependently induced PE, which was blocked by HOE140, CGRP8-37, AH-6809, and mepyramine. It was also inhibited by nociceptin, which could be reversed by antagonist J-113397. In contrast, 5-hydroxytryptamine-induced PE was biphasically regulated by nociceptin and was not antagonized by CGRP8-37.ConclusionsBK-induced PE is mediated by B2 receptors and may involve CGRP, prostaglandin, and histamine pathways. BK-induced PE is inhibited by nociceptin through the activation of ORL1 receptors. There are differences between BK- and 5-hydroxytryptamine-induced inflammation in signaling and modulation.

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Section: Discussionsupporting

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Receptor mediation and nociceptin inhibition of bradykinin-induced plasma extravasation in the knee joint of the rat

et al. 2009

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“…B1R is a non-internalizing receptor, and its long-term stimulation actually leads to an increased expression (23). Several studies point to B2R involvement in chronic inflammatory processes (24,25) and their improvement by receptor antagonist treatment (26)(27)(28)(29)(30). Reports of improvement after B2R antagonist treatment include experimental models of visceral and cutaneous inflammation (31), fatal cardiocirculatory breakdown in experimental pancreatitis (32), and antigen-induced arthritis in rabbits (33,34).…”

Section: Discussionmentioning

confidence: 99%

Interactions between bradykinin (BK) and cell adhesion molecule (CAM) expression in peptidoglycan‐polysaccharide (PG‐PS)‐induced arthritis

et al. 2004

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Bradykinin (BK), a vasoactive, proinflammatory nonapeptide, promotes cell adhesion molecule (CAM) expression, leukocyte sequestration, inter-endothelial gap formation, and protein extravasation in postcapillary venules. These effects are mediated by bradykinin-1 (B1R) and-2 (B2R) receptors. We delineated some of the mechanisms by which BK could influence chronic inflammation by altering CAM expression on leukocytes, endothelium, and synovium in joint sections of peptidoglycan-polysaccharide-injected Lewis rats. Blocking B1R results in significantly increased joint inflammation. Immunohistochemistry of the B1R antagonist group revealed increased leukocyte and synovial CD11b and CD54 expression and increased CD11b and CD44 endothelial expression. B2R antagonism decreased leukocyte and synovial CD44 and CD54 and endothelial CD11b expression. Although these findings implicate B2R involvement in the acute phase of inflammation by facilitating leukocyte activation (CD11b), homing (CD44), and transmigration (CD54). Treatment with a B2R antagonist did not affect the disease evolution in this model. In contrast, when both BK receptors are blocked, the aggravation of inflammation by B1R blockade is neutralized and there is no difference from the disease-untreated model. Our findings suggest that B1R and B2R signaling show physiologic antagonism. B1R signaling suggests involvement in down-regulation of leukocyte activation, transmigration, and homing. Further studies are needed to evaluate the B1 receptor agonist's role in this model.

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Receptor‐Mediated Events in the Microcirculation

Watts¹,

Kanagy²,

Lombard³

2008

Comprehensive Physiology

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B1 and B2 antagonists and bradykinin-induced blood flow in rat skin inflammation

Abstract: The results suggest that the involvement of the inducible B1 receptor in skin inflammation site is related to the site, duration and recurrence of the injury condition.

Cited by 6 publications

References 27 publications

Receptor mediation and nociceptin inhibition of bradykinin-induced plasma extravasation in the knee joint of the rat

Receptor mediation and nociceptin inhibition of bradykinin-induced plasma extravasation in the knee joint of the rat

Interactions between bradykinin (BK) and cell adhesion molecule (CAM) expression in peptidoglycan‐polysaccharide (PG‐PS)‐induced arthritis

Receptor‐Mediated Events in the Microcirculation

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