ABSTRACT
As autocoids, bradykinin and kallidin increase vascular permeability, produce vasodilation, increase the synthesis of prostaglandins, and cause edema and pain. Extensive evidence exists that bradykinin and other kallidin substances contribute to the pathogenesis of the inflammatory response that occurs in acute and chronic diseases, including allergic reactions, arthritis, asthma, sepsis, viral rhinitis, and inflammatory bowel diseases. Bradykinin (Arg-Pro-Pro-Gly-PheSer-Pro-Phe-Arg), a nonapeptide, and kallidin, a decapeptide, are derived from kininogens. Both tissue and plasma kallikreins are involved in the synthesis of bradykinin and kallidin (Figure 30), and both have a short plasma half-life of only 15 seconds. The kinins are catabolized by kininase II, which is also known as angiotensin-converting enzyme (see Figure 24). Kinin receptors are classified as either kinin B
or kinin B
. Kinin-B
receptors, which are located in the aorta and mesenteric veins, respond to kinin agonists in the following order of potency:
des Arg
-kallidin
>
des Arg
-bradykinin
>
kallidin
>
[try(Mc
)] bradykinin.
