Stroke is the third leading cause of death and the leading cause of disability in the Western world. Every year approximately 800,000 people experience stroke, whether it is the primary or recurrent stroke. Today, fibrinolysis is the only therapy applied in stroke patients, which is an option for a limited number of patients. In ischemic stroke, the kinin-kallikrein system is one of the first inflammatory pathways activated after ischemic tissue damage. Bradykinin concentrations as well bradykinin receptors expression significantly rise during stroke. One of the most important and most commonly reported effects of bradykinin in ischemic stroke is its effect on blood-brain barrier vascular permeability. Bradykinin expands the size of cerebral edema by increasing vascular permeability and vasodilation, significantly exacerbating the ischemic damage. Microglia and astrocytes play a significant role in the development of ischemic stroke. Their interaction with bradykinin cause various inflammatory and antiinflammatory effects. Bradykinin stimulates cytokine and chemokine secretion, acts as a leukocyte chemoattractant, promotes platelet adhesion and exacerbates inflammatory damage, but also inhibits the production of proinflammatory cytokines, stimulates migration of repair cells to the site of injury and participates in repair and regeneration of the ischemic damage. Kallikrein, forming kinins, induces angiogenesis, neovascularization and regenerates the disturbed blood flow. Moreover, kallikrein reduces ischemically induced apoptosis and oxidative stress. In conclusion, the activation of bradykinin receptors in ischemic stroke causes various deleterious but also neuroprotective effects, primarily depending on the time elapsed since the onset of ischemia and the degree of ischemia.