Effects of splanchnic nerve stimulation and of clonidine on gastric and duodenal HCO‐3secretion in the anaesthetized cat

Experiments were performed on chloralose‐anaesthetized cats with ligated adrenals. The vagal and splanchnic nerves were cut and arranged for peripheral electric stimulation. The gastric lumen was perfused with isotonic saline and gastric H+and HCO3‐secretions were calculated from pH/pCO2measurements in the perfusate. Gastric motility was recorded as changes in hydrostatic pressure in the perfusion circuit. Mucosal HCO3‐secretion into the duodenum was monitoredin situby pH‐stat titration. Vagal stimulation (10 Hz for 10 min) increased gastric and duodenal HCO3‐secretions, as well as gastric motor activity and H+secretion. Splanchnic nerve stimulation (10 Hz for 10 min) did not affect gastric H+and HCO3‐secretions, but tended to decrease gastric motor tone and basal duodenal HCO3‐secretion. Splanchnic nerve stimulation simultaneously with vagal stimulation inhibited gastric contractions and the rise in gastric H+and duodenal HCO3‐secretions observed in response to vagal stimulation alone, but had little effect on the rise in gastric HCO3‐secretion. However, such vago‐splanchnic stimulation in the presence of the α2‐adrenoceptor blocker yohimbine induced gastric contractions, H+secretory and duodenal HCO3‐secretory responses with magnitudes similar to those induced by vagal stimulation alone, whereas the gastric HCO3‐secretory response was larger than by vagal stimulation alone. The α2‐adrenoceptor agonist clonidine (50 μg kg‐1h‐1, i.v.) inhibited the gastric contractions and increases in gastric and duodenal HCO3‐secretion in response to vagal stimulation, but did not influence vagal stimulation of gastric H+secretion. The results suggest the existence of a peripheral sympatho‐inhibitory action on gasmc and duodenal HCO3‐secretion involving α2‐adrenoceptors. Also splanchnic neural stimulatory effects on gastric and duodenal HCO3‐secretion may exist.