Figure 1.

Kallikrein–kinin system (KKS). The KKS is initiated by factor XIIa (FXIIa) or prolylcarboxypeptidase on the endothelial cell and leukocyte (polymorphonuclear cell (PMN)) surface, generating the enzyme kallikrein, which in turn cleaves high-molecular-mass kininogen (HK) to yield bradykinin (BK) and cleaved high-molecular-mass kininogen (HKa). Kallikrein is chemotactic, aggregates neutrophils, and stimulates the release of elastase and superoxide (potent inducers of tissue injury). BK stimulates vasodilation, mediates pain through the release of prostaglandins, and stimulates vascular permeability through the generation of nitrous oxide (NO). PK, prekallikrein.