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A role for endogenous angiotensin II and its AT1 and AT2 receptor subtypes for mediating drinking elicited by eating was examined in adult male Sprague-Dawley rats. The ability of pharmacological antagonism of AT1 and/or AT2 receptors to abolish drinking elicited by exogenous angiotensin II was established first. The s.c. injection of the AT1 antagonist losartan (DuP 753) was sufficient to abolish drinking elicited by s.c. angiotensin II. The ICV injection (through a surgically implanted chronic cannula) of losartan inhibited drinking elicited by ICV angiotensin II; the combined ICV injection of losartan plus the AT2 antagonist PD123319 was sufficient to abolish drinking elicited by ICV angiotensin II. For rats drinking and eating after 24-h food deprivation, s.c. losartan plus PD123319 inhibited water to food ratio, but ICV losartan and/or PD123319 failed to inhibit food-related drinking. For nondeprived rats eating a small cracker, s.c. losartan and/or PD123319 attenuated water intake, but only ICV losartan produced statistically significant inhibition of drinking elicited by ingestion of cracker. The IG infusion (through a surgically implanted gastric catheter) of 2 ml 600 or 900 mOsm/kg NaCl, a treatment that is subthreshold for increase in systemic plasma osmolality at the initiation of drinking, elicited drinking that was attenuated by s.c. losartan and/or PD123319 and attenuated by ICV losartan only. The IG infusion of 2 ml 1800 mOsm/kg NaCl, a treatment that is above threshold for increase in systemic plasma osmolality at the initiation of drinking, elicited drinking that was not inhibited by S or ICV losartan and/or PD123319. These results demonstrate that peripheral AT1 and AT2 and central AT1 receptors for angiotensin II contribute to drinking elicited by eating and the gastrointestinal osmotic consequences of eating. These findings extend the evidence demonstrating a renal renin-angiotensin contribution to food-related drinking in rats.