Effects of adrenoceptor antagonists on vagally induced gastric and duodenal HCO3- secretions in the cat.

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.