Stroke is responsible for 10% of all deaths worldwide, and there remains an urgent need for the development of clinically effective treatments for acute stroke. Stroke is now considered to be a disease characterized by an ongoing inflammatory process rather than simply acute neurodegeneration. Bradykinin has attracted recent interest as a potential mediator of brain injury following stroke, because it activates several mechanisms responsible for the early manifestations of inflammation, including arteriolar dilatation, increased vascular permeability and oedema formation. These actions of bradykinin occur via activation of B(2) receptors. New evidence suggests that blocking bradykinin B(2) receptors after experimental cerebral ischaemia reduces brain oedema, infarct volume and neuronal necrosis, and improves neurological outcome. Thus, B(2) receptor antagonists may be a promising new class of compounds for clinical use after the onset of cerebral ischaemia.