Male albino rabbits received continuous (24 hr/day) infusions of angiotensin II (AH) at doses of 1 or 3 Mg/hr into a lateral cerebral ventricle (i.v.t.) for 10 consecutive days. Infusions were preceded by a 5- day control period and followed by a 5-day recovery period. Water intake, urine output, water “balance” (water intake minus urine output), urinary sodium and potassium excretions were determined daily. Arterial pressure, heart rate, plasma electrolytes (sodium and potassium), plasma volume, and extracellular fluid volume were determined at 5-day intervals. Chronic i.v.t. infusion of AH resulted in reversible, dose-dependent increases in arterial pressure, water intake, and urinary sodium excretion, and decreases in plasma sodium, plasma potassium, and water balance. Infusions of normal saline i.v.t. (n = 5) did not significantly alter any of the above values. Intravenous infusion of the same doses of AH raised arterial pressure to a similar degree as that from i.v.t. administration, but did not significantly affect any of the other measured variables. In an additional group of 10 rabbits, AH was infused at 3 μg/hr i.v.t. for 5 days, and the acute cardiovascular actions of i.v.t. saralasin (10 fig), i.v. saralasin (4 μg/kg/min), and “total” autonomic blockade were compared to the effects of these treatments in five saline-infused rabbits. No significant differences in responses of the two groups were found. In another series of 10 rabbits, 5-day i.v.t. infusion of All (3 μg/hr) was shown to be associated with increased pressor sensitivity to norepinephrine, but not to AH or vasopressin. A similar experiment in four additional rabbits revealed that plasma vasopressin concentration was not altered by i.v.t. infusion of AH. We conclude that chronic i.v.t. infusion of AH in rabbits can cause a sustained hypertension that is not dependent on salt or water retention, “leak” of AH into the peripheral vasculature, increased release of vasopressin in the circulation, or increased autonomic nervous system activity.