Angiotensin II (ANG II) attenuates baroreflex sensitivity through central pathways. However, the specific CNS sites where ANG II inhibits baroreflexes are not completely understood. The periventricular tissue of the anteroventral third cerebral ventricle (AV3V) mediates several responses to centrally and peripherally administered ANG II. Therefore, these studies determined the effects of bilateral electrolytic ablation of AV3V periventricular tissue on reflex-induced changes in heart rate during pressor and depressor responses evoked by IV administration of phenylephrine (PE), ANG II, and nitroprusside (NP). Animals were prepared with catheters in the femoral artery and vein 10-14 days following AV3V ablation or control (CONT) surgery. The following day, baroreflex sensitivity in the conscious animals was evaluated as the slope of the regression line relating blood pressure and heart rate during IV infusion (1 min) of three doses of PE, ANG II, and NP. Baroreflex sensitivity during PE and NP infusion were equivalent in AV3V-lesioned and CONT animals. However, animals with AV3V lesions demonstrated significantly greater baroreflex sensitivity during ANG II infusion than both PE-treated AV3V-lesioned animals and ANG II-treated CONT animals. These data suggest that the impairment of baroreflex-induced bradycardia during pressor responses evoked by ANG II is mediated by tissue located in the AV3V region.