L-Isoproterenol was infused at a dose of 20 pmol/kg/min for 10 min into the cranial pancreaticoduodenal artery in anesthetized dogs. Arterial plasma glucose, blood flow, and plasma concentrations of both glucagon and insulin in the cranial pancreaticoduodenal vein were significantly enhanced during the infusion, resulting in a greater increase of bihormonal output. Intrapancreatic pretreatment with propranolol abolished all of the isoproterenol-induced increases except for glucagon secretion which was suppressed only in part. Pretreatment with practolol, a specific receptor blocker of the beta1 type, did not exert any discernible inhibiting effect upon the isoproterenol-induced enhancement. Intrapancreatic infusion of trimetoquinol, a selective receptor stimulant of the beta2 type in some mammals, at an equimolar dose caused similar increases in plasma glucose, pancreatic venous blood flow, and bihormonal output when compared to those induced by isoproterenol. Pretreatment with a larger dose of propranolol totally abolished the trimetoquinol-induced enhancement of both glucagon and insulin secretion. Pretreatment with an isomolar dose of practolol, in contrast, did not show any suppressive effect on the parameters investigated. There was a dose-dependency in the bihormonal responses to trimetoquinol. Another beta2 receptor agonist, salbutamol, also significantly raised plasma glucose, pancreatic venous blood flothough to a lesser extent than did trimetoquinol. These results indicate that the adrenergic control over the function of the endocrine pancreas through beta adrenoreceptors may be mediated mainly via those of the beta2 type.