Cessation of blood flow in tissues leads to depletion of energetic resources of cells, disturbances in the activity of enzymes of the oxidative chain and electrolyte disorders, as well as to the production of reactive oxygen species. A great deal of attention has been paid to those problems since they are responsible for most of the complications in the ischemia-reperfusion (I/R) syndrome. Understanding the antioxidative mechanisms involved in I/R syndrome provides us with the potential to correct at least some of the resulting disturbances. One of the potentially beneficial factors is insulin. This observation directed our attention to the insulin-like factors, kinins (especially bradykinin), the activation of which was detected in I/R syndrome. The effect of bradykinin is modified by concurrent administration of the specific antagonists of bradykinin receptors, B1 and B2. The aim of the current study was to assess the role of bradykinin. In the study, the employed agents included the angiotensin converting enzyme inhibitor, which prevents the degradation of endogenous kinins, and blockers of bradykinin receptors, which abolish the influence of kinins. We observed that after 4 hours of ischemia followed by reperfusion, levels of free radicals in tissues as well as levels of peroxides in plasma increased significantly. Administration of bradykinin, captopril or enalapril resulted in the decline of these free radical levels. The application of B2 receptor antagonist decreased the beneficial influence of bradykinin, whereas B1 receptor antagonist revealed no significant effect. Activities of antioxidative enzymes (superoxide dismutase, catalase, and glutathione peroxidase) were measured. After 4 hours of ischemia and consecutive steps of reperfusion, a statistically significant increase in their activities was observed when bradykinin or ACE inhibitors were administered. Application of B2 receptor blockers reduced the effect of bradykinin, whereas the effect of B1 receptor antagonists was minute.