Experimental allergic encephalomyelitis (EAE) is a delayed cell-mediated autoimmune reaction to myelin basic protein. The neuropathology of this acute inflammatory process is characterized by cellular infiltration of the perivascular nervous parenchyma which increases the blood-brain barrier permeability. There is good evidence for an activation of the kallikrein-kinin system during inflammation. In order to assess blood concentrations of kinins in a group of 21 New Zealand rabbits in the acute phase of EAE and a group of 12 normal controls, we performed a sensitive and specific radioimmunoassay. All subjects in the encephalomyelitic group were inoculated with 0.05 ml of an antigenic preparation. They all developed neurological deficits on average 30 days later and within 4 days 10 ml of arterial blood were withdrawn for radioimmunoassay of kinins. On the same days their central nervous system was dissected and prepared for staining and histological study. We demonstrated a significant difference in bradykinin blood concentration between the encephalomyelitic (170.6 pg/ml) and the control (245.8 pg/ml) groups. There is also a significant difference in des-Arg9-bradykinin blood concentration between the encephalomyelitic (168.0 pg/ml) and the control (96.1 pg/ml) groups. These results suggest an activation of circulating carboxypeptidases involved in the transformation of bradykinin into des-Arg9-bradykinin during EAE.