Cockerels of an egg-laying strain were used to study the mode of action of epinephrine on food intake in chickens. Intraperitoneal injection of 2500 micrograms epinephrine significantly depressed intake from 1-6 hr after injection. This effect was not modified by vagotomy at the level of the proventriculus (equivalent of subdiaphragmatic vagotomy in the mammal). Injection of 25, 50 or 100 micrograms epinephrine into the hepatic portal vein depressed intake in a dose-related manner. One hundred micrograms epinephrine had similar effects when injected into the jugular vein as into the portal vein, although the latter injection had longer-lasting effects. As the liver is the major site of inactivation of epinephrine this suggests that it acts mainly at that organ. In order to find which type of receptor is stimulated by epinephrine in its action on feeding an alpha-adrenergic agonist, phenylephrine, was injected into the portal vein at doses ranging from 63-3000 micrograms; there was no effect on intake at any dose. A beta-adrenergic agonist, salbutamol (500-2000 micrograms), depressed intake in a dose-related manner following portal vein injection. This effect was not attenuated by vagotomy. Aminophylline, an inhibitor of cAMP breakdown, had no effect on intake when injected into the portal vein (2500-10000 micrograms) and the depressing effect of 200 micrograms epinephrine was not modified by simultaneous injection of 10000 micrograms aminophylline. It is concluded that epinephrine acts on the liver to suppress intake via a vagally-mediated pathway, but that the mechanisms of action are not known.