Increased sodium intake is somehow induced in rats by intravenous angiotensin II

Adult male rats maintained on dry food, water, and 3% NaCl solution received continuous infusion of angiotensin II (A II) via right atrial catheters. A II was delivered in 0.315 ml/hr at doses of 15, 30, and 60 ng/min/rat for 3 to 5 days. At the higher doses mean daily salt solution intake rose from very low preinfusion levels to 18.7 and 19.6 ml, respectively. Daily water intakes increased in some animals and decreased in others on the first day of infusion but were double preinfusion levels by the second day. Persistence of the sodium appetite after the end of A II infusion was seen in most of the rats which received the highest dose. The mechanisms which might underlie the effect of blood-borne A II on sodium intake are discussed and three possibilities considered: (1) that A II may act on the brain to stimulate sodium appetite, (2) that A II may act via the adrenal cortex, and that the sodium appetite may arise as a result of increased plasma levels of adrenal steroids, and (3) that A II may act via the kidney, producing a natriuresis. According to this view, sodium appetite would arise as a result of loss of body sodium and/or blood volume.