The role of the adrenergic system in the duodenal mechanisms that inhibit gastric acid secretion (GAS) after duodenal acidification (DA) was studied. In 12 mongrel dogs, with gastric and duodenal fistulas, six experiments were carried out evaluating penta-gastrin-stimulated GAS and serum secretin levels: DA (HC12 ml/min) for 1 h (group A); DA (HC12 ml/min) for 1 h plus propranolol (group B); DA (HC1 2 ml/min) for 1 h plus phentolamine (groupt C); duodenal instillation of saline (2 ml/min) for 1 h (group D); (duodenal instillation of saline (2 ml/min) for 1 h plus propranolol (group E), and duodenal instillation of saline (2 ml/min) for 1 h plus phentolamine (group F). Significantly (p < 0.05) high percentages of inhibition of GAS (49–70.5%) paralleled with increases of serum secretin levels (48.4–84%) were noted in group A and C experiments. However, DA did not inhibit GAS nor did it increase the levels of secretin in group B and D-F experiments. It is concluded that the inhibition of GAS after DA is controlled, at least in part, by the action of the β-adrenorecep