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- W2111776883 abstract "The involvement of bradykinin (BK) receptors in the allergic inflammation associated with airway hyper-reactivity (AHR) was evaluated by means of the selective bradykinin B1 receptor (BKB1-R) antagonists R-715 (Ac-Lys-[D-βNal7, Ile8]desArg9-BK) and R-954 (Ac-Orn[Oic2, α-MePhe5, D-βNal7, Ile8]desArg9-BK) or the selective bradykinin B2 receptor (BKB2-R) antagonist HOE-140 (D-Arg0-Hyp3-Thi5-D-Tic7-Oic8-BK). Cellular migration and AHR were examined 24 h after the second ovalbumin (OA) challenge. R-715 (10–500 μg kg−1) and R-954 (1–100 μg kg−1) injected intravenously (i.v.), 5 min prior to aerosol OA challenges, decreased by approximately 50% the induced lung eosinophilia in OA-sensitized mice but did not reduce AHR. HOE-140 (1 μg kg−1) administered in the same manner, decreased mononuclear cell and eosinophil infiltration in the bronchoalveolar lavage fluid (BALF) of OA-sensitized mice. Moreover, treatment of OA-sensitized mice with HOE-140 (100 μg kg−1) completely abolished the AHR to carbachol. The BKB1-R agonist desArg9-BK (DBK; 10–1000 μg kg−1) administered intratrachealy to normal mice had no effect on the basal cell counts recovered in BALF nor on the plasma extravasation, while the BKB2-R selective agonist BK (20 μg kg−1) stimulated mononuclear cell migration, neutrophilia and plasma extravasation in normal mouse lungs. Such effects were inhibited by HOE-140 (10 μg kg−1). Our results suggest that the airway inflammatory response induced by antigen challenge in mice is mediated by stimulation of both BKB1-R and BKB2-R. British Journal of Pharmacology (2003) 138, 1589–1597. doi:10.1038/sj.bjp.0705207" @default.
- W2111776883 created "2016-06-24" @default.
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- W2111776883 date "2003-04-01" @default.
- W2111776883 modified "2023-09-23" @default.
- W2111776883 title "Implication of the bradykinin receptors in antigen-induced pulmonary inflammation in mice" @default.
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- W2111776883 doi "https://doi.org/10.1038/sj.bjp.0705207" @default.
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