SUMMARY Intraventricular administration of angiotensin II (AII), 1 μg, twice a day for 2 weeks, together with saline as the drinking fluid during the second week, resulted in moderate but significant elevation of the arterial pressures of mongrel dogs. This increase in arterial pressure was accompanied by a significant elevation in femoral and renal vascular resistances. However, resting neurogenic tone to the hind limb vasculature and peripheral sympathetic transmission to renal and femoral vascular beds were not altered by AH treatment, indicating that the elevation of intrinsic vascular tone of the smooth muscle was responsible for elevated vascular resistance in the hind limb vasculature. Furthermore, pressor responses to intravenous (I.V.) norepinephrine and angiotensin II were enhanced. Also, reflexly mediated vasodilator responses were attenuated in the hind limb, and vascular responses to infra-arterial and I.V. doses of histamine were reduced. However, blood pressure responses to bilateral carotid occlusion and intra-arterial and I.V. responses to acetylcholine and bradykinin were unaffected. The concentration of urinary sodium was significantly greater in the All-treated group. The data from this investigation indicate that chronic cerebrolateral ventricular administration of angiotensin II (plus saline) to mongrel dogs resulted in certain vascular alterations that are conducive to the development of high blood pressure.