Dissociation of dipsogenic and pressor responses to chronic central angiotensin II in rats

Chronic intracerebroventricular (icv) infusion of angiotensin II (ANG II) (6 micrograms/h) in rats resulted in a sustained 70-mmHg rise in blood pressure during 7 days of treatment. A marked dipsogenic response preceded the maximal rise in blood pressure, peaked at 24 h, and returned to control by the 5th day. Urinary sodium excretion rose on the 1st day of infusion but thereafter was not different from that of vehicle-infused rats. ANG II-infused rats showed a small but significant kaliuresis, a fall in serum osmolality (5.5 mosmol/kg), but no change in plasma Na+, K+, or glucose. Rats infused with the same dose of ANG II intravenously showed a small, 8-mmHg rise in blood pressure, but none of the changes noted after icv ANG II. Plasma renin activity was suppressed in rats infused with ANG II by both routes. We conclude that the pressor, dipsogenic, and renal excretory effects of icv ANG II are mediated centrally and cannot be explained by leakage of the peptide into the systemic circulation. Furthermore, the pressor and dipsogenic effects of ANG II become clearly dissociated during chronic icv infusion.