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Blockade of central angiotensin receptors with the specific antagonist [Leu8]-ANG II abolished water ingestion and water and sodium excretion induced by infusion of angiotensin II (ANGII) into the lateral ventricle (LV) of rats. The antagonist reduced but did not suppress the salt appetite induced by ANGII infusion. Subcutaneous injection of deoxycorticosterone acetate (DOCA) caused increases in water and 3% NaCl ingestion and decreases in sodium excretion. When central ANGII infusion was combined with peripheral DOCA, the water intake was similar to that induced by ANGII alone and the ingestion of 3% NaCl was increased, whereas sodium excretion was inhibited. When ANGII was infused alone, a detailed temporal analysis of fluid and sodium balance showed a negative balance similar those saline controls that persisted throughout the experiment. Combined administration of ANGII and DOCA induce significant changes in water and sodium balance. Sodium and water maintained a positive balance through out the 8-h experiment. The data support an interaction of central ANGII and DOCA on sodium intake and water and sodium balance.

Because the anteroventral wall of the third ventricle (AV3V) has been implicated in the control of sodium intake it was studied in rats with damage of the AV3V region in the sodium-replete and sodium-deplete states, and when they were treated with either pulse intracerebroventricular (pICV) injection of renin to activate brain angiotensin or daily subcutaneous injections of deoxycorticosterone (DOCA). The response of rats with AV3V damage to sodium depletion was retarded and the excess sodium intake that is induced by pICV renin was absent, but their daily need-free sodium intake and the sodium intake that is induced by DOCA were essentially normal. The results suggest that the AV3V is responsible for the angiotensinergic, but not the aldosteronergic, component of the ANG II/ALDO synergy that controls need-induced sodium appetite in the rat. The integrity of the AV3V is not necessary for daily need-free sodium intake or for its enhancement by sodium depletions, suggesting that ANG II is probably not important for these phenomena. But ANG II action within the AV3V might be important for the rapid burst of sodium intake that immediately follows a period of depletion.

Studies were carried out in the dog to determine the extent to which alterations in total body sodium influence the systemic conversion of angiotensin 1. When the animals were maintained on a high salt diet and DOCA, conversion of angiotensin I increased signifcantly and returned to control levels when a normal salt diet was provided. When another group of animals were provided a low salt diet and mercuhydrin, angiotensin I conversion decreased significantly, although returning the animals to a normal salt diet had no further influence upon conversion. These experiments indicate that there is a direct relationship between total body sodium and the systemic conversion angiotensin 1.