Role of the kallikrein-kinin system in inflammation has been studied in rat model of inflammation, such as paw edema and pleurisy. Previous works suggested involvement of HMW-kininogen and activation of plasma kallikrein system in the carrageenin-induced rat pleurisy at early phase. This study clearly demonstrates the involvement of HMW-kininogen in carrageenin-induced rat paw edema and carrageenin-induced rat pleurisy by using congenitally deficient rat strain in plasma HMW-kininogen. Conclusion is the followings: 1. Significantly less reactivity was noticed in the deficient strain, B/N-Ka, in comparison with normal strain, B/N-Ki, when carrageenin-paw edema or carrageenin- and kaolin-pleurisies were induced. 2. Pretreatment with captopril enhanced the paw swelling as well as pleural fluid accumulation in normal strain but no enhancement was observed in the deficient strain. These results indicate that HMW-kininogen is responsible to inflammatory exudation. 3. T-kinin may not be involved in these inflammations, since the deficient strain owns normal plasma level of T-kininogen.