Effects of chronic intracerebroventricular infusion of angiotensin II on arterial pressure and fluid homeostasis.

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Abstract
Male albino rabbits received continuous (24 h/day) infusions of angiotensin II (AII) at doses of 1 or 3 .mu.g/h 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 Na and K excretions were determined daily. Arterial pressure, heart rate, plasma electrolytes (Na and K), plasma volume, and extracellular fluid volume were determined at 5-day intervals. Chronic i.v.t. infusion of AII resulted in reversible, dose-dependent increases in arterial pressure, water intake and urinary Na excretion and decreases in plasma Na , plasma K and water balance. Infusions of normal saline i.v.t. (n = 5) did not significantly alter any of the above values. I.V. infusion of the same doses of AII raised arterial pressure to a similar degree as that from i.v.t. administration, but did not significantly affect any of the other measured variable. In an additional group of 10 rabbits, AII was infused at 3 .mu.g/h i.v.t. for 5 days, and the acute cardiovascular actions of i.v.t. saralasin (10 .mu.g), i.v. saralasin ( 4 .mu.g/kg/min), and total autonomic blockade were compared to the effects of these treatments in 5 saline-infused rabbits. No significant differences in responses of the 2 groups were found. In another series of 10 rabbits, 5-day i.v.t. infusion of AII (3 .mu.g/h) was associated with increased pressor sensitivity to norepinephrine, but not to AII or vasopressin. A similar experiment in 4 additional rabbits revealed that plasma vasopressin concentration was not altered by i.v.t. infusion of AII. Chronic i.v.t. infusion of AII in rabbits can cause a sustained hypertension that is not dependent on salt or water retention, leak of AII into the peripheral vasculature, increased release of vasopressin in the circulation, or increased autonomic nervous system activity.