• J P Wang, M F Hsu, C H Ouyang, and C M Teng.
• Pharmacological Institute, College of Medicine, National Taiwan University, Taipei, Taiwan.
• Eur. J. Pharmacol. 1989 Feb 28;161(2-3):143-9.

Abstract[Thi5,8,D-Phe7]bradykinin caused hind-paw edema and degranulation of isolated peritoneal mast cells in a dose-dependent manner. Pretreatment with diphenhydramine/methysergide or compound 48/80 completely suppressed the edematous response caused by [Thi5,8,D-Phe7]bradykinin, whereas bradykinin-induced hind-paw swelling was only partially inhibited by diphenhydramine and methysergide pretreatment; the residual response was significantly further depressed by [Thi5,8,D-Phe7]bradykinin. Neither the bradykinin- nor [Thi5,8,D-Phe7]bradykinin-induced edematous response was significantly affected by aspirin or BW755C. The mast cell degranulation caused by [Thi5,8,D-Phe7]bradykinin and bradykinin was inhibited by gangliosides but not by heparin. These results suggest that the edematous response elicited by [Thi5,8,D-Phe7]bradykinin was mainly due to the actions of mediators released by the degranulation of mast cells. Unlike bradykinin, [Thi5,8,D-Phe7]bradykinin was devoid of a direct exudation-promoting effect but exerted an antagonistic effect on the direct effect of kinin. If the influence of mast cells degranulation could be minimized, [Thi5,8,D-Phe7]bradykinin could be used as a tool to evaluate the role of kinin in the edematous response in inflammation.

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