ANGIOTENSIN AT(1) AND AT(2) RECEPTORS CONTRIBUTE TO DRINKING ELICITEDBY EATING IN RATS

A role for endogenous angiotensin II and its AT(1), and AT(2) receptor subtypes for mediating drinking elicited by eating was examined in ad ult male Sprague-Dawley rats. The ability of pharmacological antagonis m of AT(1) and/or AT(2) receptors to abolish drinking elicited by exog enous angiotensin II was established first. The SC injection of the AT (1) antagonist losartan (DuP 753) was sufficient to abolish drinking e licited by SC 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 AT (2) antagonist PD123319 was sufficient to abolish drinking elicited by ICV angiotensin II. For rats drinking and eating after 24-h food depr ivation, SC 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, SC losartan and/or PD1233 19 attenuated water intake, but only ICV losartan produced statistical ly 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 in crease in systemic plasma osmolality at the initiation of drinking, el icited drinking that was attenuated by SC 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 pl asma osmolality at the initiation of drinking, elicited drinking that was not inhibited by SC or ICV losartan and/or PD123319. These results demonstrate that peripheral AT(1) and AT(2) and central AT(1) recepto rs for angiotensin II contribute to drinking elicited by eating and th e gastrointestinal osmotic consequences of eating. These findings exte nd the evidence demonstrating a renal renin-angiotensin contribution t o food-related drinking in rats.