Angiotensin II (ANG II) attenuates baroreflex sensitivity through cent
ral pathways. However, the specific CNS sites where ANG II inhibits ba
roreflexes are not completely understood. The periventricular tissue o
f the anteroventral third cerebral ventricle (AV3V) mediates several r
esponses to centrally and peripherally administered ANG II. Therefore,
these studies determined the effects of bilateral electrolytic ablati
on of AV3V periventricular tissue on reflex-induced changes in heart r
ate during presser and depressor responses evoked by IV administration
of phenylephrine (PE), ANG II, and nitroprusside (NP). Animals were p
repared with catheters in the femoral artery and vein 10-14 days follo
wing AV3V ablation or control (CONT) surgery. The following day, baror
eflex sensitivity in the conscious animals was evaluated as the slope
of the regression line relating blood pressure and heart rate during I
V infusion (1 min) of three doses of PE, ANG II, and NP. Baroreflex se
nsitivity during PE and NP infusion were equivalent in AV3V-lesioned a
nd CONT animals. However, animals with AV3V lesions demonstrated signi
ficantly greater baroreflex sensitivity during ANG II infusion than bo
th PE-treated AV3V-lesioned animals and ANG II-treated CONT animals. T
hese data suggest that the impairment of baroreflex-induced bradycardi
a during presser responses evoked by ANG II is mediated by tissue loca
ted in the AV3V region.