The actions of bradykinin on pial venule leaky site formation were measured intra-vitally in two inbred strains of mice (BALB/c and SJL/J). Pial venules were visualized using an open cranial window microscopy technique and the microvascular leaky site formation was assessed visually using a fluorescein-dextran (70 kDa) indicator. The SJL/J strain was found to be very sensitive to bradykinininduced microvascular leakage. Pial venule leaky site formation was observed after exposure to 10 p M of bradykinin. In contrast, the BALB/c strain was found to be refractory to bradykinin-induced leakage. Pial arterioles were dilated in response to bradykinin in both strains of mice. These results support the concept that genetically controlled differences in vascular sensitivity and localization of inflammatory peptides play important roles in the generation of vasogenic oedema and inflammation in CNS trauma and disease.