The effect of bradykinin on cerebrovascular resistance vessels was investigated by the use of in vitro and in situ preparations. Bradykinin, in the range of 10(-10) to 10(-5) M, elicited a concentration-dependent vasodilatation on both feline and human pial arteries in vitro; the half-maximal response was found to be approximately at 2.8 X 10(-7) M and 1.3 X 10(-8) M (EC50), respectively. This dilatatory effect of bradykinin in vitro was found only in arteries preconstricted with prostaglandin F2 alpha or 5-hydroxytryptamine. In order to determine the effects of bradykinin on the diameter of cat pial arteries in situ, perivascular microapplication was employed. The dose-response curves obtained showed vasodilatation; the EC50 and the maximal response (EAm) were 4.4 X 10(-7) M and 45.5% at 10(-5) M, respectively. Statistically significant (p less than 0.01) reactions were observed at 10(-7) M and higher concentrations of bradykinin. The observed effects were independent of initial vessel size (80-260 microns). These in situ findings are very similar to those found in vitro. The isolated guinea pig ileum was used to check the stability of the bradykinin solutions. In this instance, a concentration-dependent contraction was found when "freshly prepared" or "5 hours stored" bradykinin was applied, indicating no measureable degradation of bradykinin. We conclude that bradykinin is a powerful vasodilator of both human and feline pial arteries.