Angiotensin II mediates drinking elicited by eating in the rat.

Captopril (CA) was used to block synthesis of endogenous angiotensin II (ANG II) in periphery and/or brain of adult male Sprague-Dawley rats in tests for drinking elicited by eating pelleted chow. Blockade of ANG II-converting enzyme (ACE) in periphery alone (using 0.5 mg/kg CA) increased drinking elicited by eating, whereas simultaneous blockade of ACE in periphery and brain (using subcutaneous 100 mg/kg CA or subcutaneous 0.5 mg/kg plus third ventricular 25 micrograms CA) decreased such drinking. The inhibitory effect of 100 mg/kg CA on water-to-food ratio was prevented by a dipsogenically subthreshold subcutaneous dose (5 micrograms/kg) of ANG II. Blockade of ACE in brain alone (third ventricular 25 micrograms CA) had no effect on food-related drinking. Pharmacological antagonism of ANG II (100 mg/kg CA) together with antagonism of histamine H1 and H2 receptors (using intraperitoneal dexbrompheniramine and cimetidine) were not additive in their inhibitory effects on drinking elicited by eating. Blockade of ACE (100 mg/kg CA) inhibited drinking elicited by subcutaneous histamine, but blockade of histamine receptors failed to inhibit drinking elicited by subcutaneous ANG II. These results support a role for endogenous ANG II under what appear to be physiological conditions for drinking behavior, i.e., when drinking is elicited by eating, and they suggest the working hypothesis of ANG II mediation of a histaminergic mechanism for food-related drinking in the rat.