A–C, Slow-pressor AngII hypertension enhances AVP immunoreactivity (A) and increases the number of AVP-positive cells in the PVN at 14 d (*p < 0.05 from saline; n = 5 per group) (B). Plasma AVP is also elevated at 14 d (C) (*p < 0.05 from saline; n = 5 per group). C, Adenoviral gene transfer of CuZnSOD (AdSOD) in SFO prevents the plasma AVP increase. D–F, Administration of the V1a AVP receptor antagonist SR49059 (4 mg/100 ml in drinking water, days 7–14 of AngII infusion) attenuates resting systolic AP, but does not prevent the AP rise induced by AngII. D, Systolic AP was measured by tail cuff plethysmography (*p < 0.05 form respective saline group; # p < 005 from vehicle; n = 6 per group). E, F, SR49059 (SR) partially prevents the attenuation in the response to whisker stimulation (E) or topical application of acetylcholine (F) induced by AngII. SR49059 + losartan (Los; 5 μm) completely prevents the attenuation (E, F) (*p < 0.05 from respective saline group; ^#p < 0.05 from vehicle, SR + Los, and respective saline group; n = 6 per group). G, Application of SR49059 (10 μm) to the cranial window does not block the attenuation of functional hyperemia induced by chronic AngII (*p < 0.05 from saline; n = 5 per group). H, The reduction in resting CBF produced by neocortical application of AVP is blocked by SR49059, either applied to the neocortex (10 μm) or administered in the drinking water for days 7–14 of AngII infusion (P.O.) (*p < 0.05 from vehicle; n = 5 per group).