1. Studies of gastric function were made in preruminant calves fitted with a single abomasal cannula, re-entrant cannulas in the duodenum close to the pylorus and recording electrodes on the pyloric antrum and proximal duodenum.
2. Simultaneous measurements were made of gastric emptying of a saline (9 g sodium chloride/1) meal, myoelectric activity of antral muscle and plasma concentration of somatostatin in jugular blood whilst infusing the duodenum with different solutions. The duodenal infusates were isotonic sodium bicarbonate (300 mosmol/kg), hyperosmolar solutions of NaCl (1000 mosmol/kg), sodium carbonate (500 mosmol/kg), sucrose (1000 mosmol/kg), 41 g emulsified butterfat/kg or 60 mM-hydrochloric acid.
3. Infusing the duodenum with isotonic NaHCO3 stimulated intense myoelectric activity of the antral smooth muscle and rapid emptying of the test meal. In contrast, infusions of 60 mM-HCl reduced antral motility and inhibited gastric emptying of digesta. This inhibitory response to HCl infusion was related to a significant (P < 0·05) increase of somatostatin in peripheral venous blood.
4. The Na2CO3 infusate, like HC1, inhibited gastric motor activity and digesta emptying, but the concentration of circulating somatostatin was only slightly elevated above pre-infusion levels.
5. Compared with the effects of infusing HCl, infusions of emulsified butterfat or hyperosmolar NaCl and sucrose induced a greater intensity of antral motor activity and faster outflow of gastric effluent, although not to the same extent as with isotonic NaHCO3. However, as with isotonic NaHCO3, these infusates did not evoke the release of somatostatin.
6. The results support the concept of duodenal receptors which, in response to a variety of stimuli in gastric chyme, modulate stomach emptying of digesta through actions on contractile processes of antral smooth muscle. Activation of such receptors by fat or osmotic stimuli, both ionic and non-ionic, do not appear to involve the release of somatostatin. However, the hormone appears to have an entero-gastrone role in mediating the inhibitory action of HCI on gastric motor function.