Experiments were performed on chloralosed cats with ligated adrenal glands. The cervical vagi were cut and arranged for electric stimulation. The gastric lumen was continuously perfused, and the secretions of H+ and HCO3- were calculated from pH/pCO2 measurements in the perfusate. Gastric motility was recorded as changes in hydrostatic pressure within the perfusion system. Mucosal HCO3- secretion into a duodenal segment, distal to the papilla of Vater and Brunners gland area, was titrated in situ by a pH-stat equipment. Animals pretreated with various adrenoceptor blockers or splanchnicotomy were compared with control animals with intact sympatho-adrenergic system. Basal gastric motor activity, H+ and HCO3- secretions, as well as duodenal HCO3- secretion were not influenced by prazosin, propranolol or splanchnicotomy. Yohimbine increased significantly basal gastric HCO3- secretion, but did not influence basal gastric motor activity, H+ secretion or duodenal HCO3- secretion. Vagal stimulation in yohimbine-treated or splanchnicotomized animals induced significantly larger gastric contractions, HCO3- secretory and duodenal HCO3- secretory responses than in the controls, whereas these responses to vagal stimulation were small in prazosin- or propranolol-treated animals. Vagally induced gastric H+ secretory responses were significantly larger in propranolol-treated animals than in controls, whereas prazosin-treated, yohimbine-treated or splanchnicotomized animals in this regard did not differ from the controls. The results suggest the existence of a sympathetic, probably alpha-2-adrenergic, inhibition of vagally induced gastric contractions as well as of the gastric and duodenal HCO3- secretions.