Food intake of domestic fowl injected with adrenergic agonists and antagonists into the hepatic portal vein

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 μg 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 μg epinephrine into the hepatic portal vein depressed intake in a dose-related manner. One hundred μg 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 α-adrenergic agonist, phenylephrine, was injected into the portal vein at doses ranging from 63–3000 μg; there was no effect on intake at any dose. A β-adrenergic agonist, salbutamol (500–2000 μg), 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 μg) and the depressing effect of 200 μg epinephrine was not modified by simultaneous injection of 10000 μg 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.