Bradykinin induced edema inhibition

It is of interest how the presently accepted concept of aspirin and aspirinlike compounds involvement with PGs came about. The last of the aspirin theories to arise proposed that aspirin interfered with leukocyte migration to the site of injury, thus inhibiting the inflammatory process. A prostaglandin phase of inflammation, where PGs arose in the exudate of experimentally induced edema after the appearance of histamine and bradykinin, was already known. These two events appeared to coincide in the inflammatory process. Thus, the time was ripe. In studying the mediators responsible for the anaphylactic response in sensitized guinea pig lungs, Piper and Vane (1969) isolated histamine, SRS-A, and a new substance they called rabbit aorta contracting substance (RCS), a very unstable material (1 to 2 min) whose release, and presumably production, was selectively inhibited by aspirin-... 

Oral administration of a total benzene extract of the aerial parts of chirata inhibited hind paw edema induced in rats by bradykinin. 

Fernandes et al. [35] reported that these SQTs were able to inhibit the activation and/or release of inflammatory mediators like bradykinin, platelet activating factor, histamine, IL, IL-1 p, TNFa, and PGE2. They also inhibited the up-regulation of the enzymes COX-2 and iNOS (inducible nitric oxide synthase). a-Humulene stood out in the study as it was the only compound that could, in a systematic treatment, reduce the histamine-induced mouse paw edema and largely prevent both TNFa... 

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