Intestinal control of gastric function in the calf: the relationship of neural and endocrine factors.

1. Gastric emptying and secretion were measured in conscious calves during alkaline or acid perfusion of the duodenum with simultaneous assessment of endogenous plasma somatostatin, gastrin and blood 5-hydroxytryptamine (5-HT).2. Alkaline duodenal perfusion (isotonic NaHCO(3)) caused rapid gastric emptying and increased gastric acid secretion without any affect on basal levels of somatostatin, 5-HT or gastrin.3. Duodenal perfusion of 60 mm-HCl caused complete inhibition of gastric emptying, reduced gastric acid secretion considerably, and an associated elevation of somatostatin basal levels from 123.8 +/- 11.2 to 281.9 +/- 23.0 pg/ml. (P < 0.01) occurred.4. These effects of duodenal perfusion were unimpaired by bilateral lumbar splanchnectomy.5. On bilateral cervical vagotomy of the splanchnectomized calves, the inhibition of gastric function evoked by duodenal acidification persisted, and plasma somatostatin showed a further significant elevation to 506.9 +/- 49.9 pg/ml. (P < 0.01) but gastrin and 5-HT remained unchanged. The increased gastric function caused by alkaline duodenal function was significantly reduced following vagotomy but basal somatostatin, gastrin and 5-HT in the blood remained unaffected.6. These results suggest that the stimulatory effect on gastric emptying and acid secretion of isotonic NaHCO(3) in the duodenum may be mediated, partially at least, through the vagal nerves but not the splanchnics.7. The complete inhibition of gastric function which ensued on acidification of the duodenum and which continues after splanchnovagotomy, is not mediated by the autonomic nervous system. This inhibitory process appears to involve the endocrine system only, with somatostatin (but not gastrin or 5-HT) fulfilling a main enterogastrone role.