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.

We also recommend Trading Suppliers and Manufacturers of bradykinin, (hydroxy-Pro)(3)-Lys- (cas 113662-39-8). Pls Click Website Link as below: cas 113662-39-8 suppliers