Bradykinin receptor antagonists in cerebral ischemia and trauma
1Department of Neurosurgery, Ludwig-Maximilians-University, Klinikum Grosshadern, Marchioninistrasse 15, 81377 Munich, Germany. Stefan.Zausinger@nc.med.uni-muenchen.de
Abstract:
Bradykinin, an endogenous nonapeptide produced by activation of the kallikrein-kinin system, promotes neuronal tissue damage as well as disturbances in blood-brain barrier function, mainly through the activation of B2 receptors. Both cerebral ischemia and trauma are associated with an activation of the kallikrein-kinin system, resulting in a sustained production of kinins. This is strong evidence supporting an involvement of bradykinin-mediated secondary brain damage following cerebral ischemia and trauma. Accordingly, specific inhibition of bradykinin B2 receptors attenuates brain swelling and limits tissue damage, indicating its potential in patients with acute cerebral ischemia and trauma.
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