Pro-inflammatory effects induced by bradykinin in a murine model of pleurisy

Add time:08/23/2019    Source:sciencedirect.com

Bradykinin caused a dose-related increase in cell influx 4 h after its administration into the mouse pleural cavity (ED50=3.2 nmol/cav., 95% confidence limits=0.6–15.5). Cell influx peaked at 4 h and remained elevated for up to 72 h, whereas exudation was detected between 2 and 6 h after bradykinin administration. Both HOE 140 (d-Arg–[Hyp3,Thi5,d-Tic7, Oic8]bradykinin) and NPC 17731 (d-Arg0–[Hyp3d–HypE(transpropyl7)Oic8]bradykinin) inhibited bradykinin-induced cell influx (ID50 0.028 (0.05–0.16) and 0.4 (0.3–0.7) pmol/cav., respectively). Des–Arg9–[Leu8]bradykinin (0.1 and 3.0 nmol/cav., 30 min before) did not inhibit the effects of bradykinin. Pre-treatment of animals with either indomethacin, terfenadine, dexamethasone, Nω-nitro-l-arginine benzyl ester, cromolyn, theophylline, salbutamol, FK 888 (N2-[(4R)-4-hydroxy-1-(1-methyl-1H-indol-3-yl)carbonyl-l-propyl]N-metyl-N-phenyl-methyl-3-(2-naphthyl)-l-alaninamide) or SR 142801 ((N)-(1-{3-[1-benzoyl-3-(3,4-dichloro-phenyl)-piperidin-3-yl]propyl}-4-phenyl-piperidin-4-yl)-N-methyl-acetamide) significantly inhibited cell migration (P<0.01). These results indicate that bradykinin had a significant pro-inflammatory effect on the pleural cavity of the mice. This effect seems to be primarily mediated via activation bradykinin B2 receptors which trigger the release of other mediators.

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