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1. Gastric emptying, gastric acid and pepsinogen secretion were assessed simultaneously in the conscious calf using the test meal and duodenal perfusion technique (Bell & Mostaghni, 1975).2. Duodenal infusion of NaCl at a constant osmolality of 300 m-osmole/kg, but with pH ranging from 2.0 to 12.0, did not alter the high level of gastric emptying and secretion already reported for isotonic NaCl or NaHCO(3) alone (Bell & Mostaghni, 1975; Bell & Webber, 1979). Gastric function, therefore, is either unaffected by gastric chyme at pH 2.0-12.0 entering the duodenum, or else isotonicity is dominant over pH in activating duodenal receptors which increase motor activity.3. When the pH of the isotonic NaCl was reduced by the addition of HCl to below pH 2.0, inhibition of gastric function occurred in direct proportion to the amount of titratable acid present in the infusate. The H(+) moiety of isotonic duodenal infusates of pH < 2.0 dominates activation of osmoreceptors and so inhibits motor activity.4. When the same amount of acid but at differing concentrations and infusion rates was introduced into the duodenum uniform inhibition of gastric function occurred. This result indicates that duodenal acid receptors respond to acid concentration and flow rate to produce an integrated response in proportion to the amount (concentration x volume) of acid present.5. Isotonic NaHCO(3) solutions adjusted to pH 8.1-12.0 by the addition of NaOH, like isotonic NaCl infusions, did not affect gastric function until pH 11.0-12.0, when significant inhibition occurred. This inhibitory effect of isotonic NaHCO(3) at high pH is probably due to CO(3) (2-), since Na(2)CO(3) and Li(2)CO(3), but not LiCl, produce a similar inhibitory effect on gastric function.6. The inhibitory effect of carbonate gives some support to the existence of a CO(2)-sensor as suggested by Hunt & Knox (1972), whereby increased P(CO2) produced by intracellular or intercellular neutralization of CO(3) (2-) by duodenal H(+) activates acid receptors. But other experiments reported here, where simultaneous perfusion of HCl and excess NaHCO(3) produced a rise in intraluminal P(CO2), did not inhibit gastric function, which is contrary to the idea of a direct intraluminal effect of CO(2) on duodenal receptors.7. The pH, P(O2), P(CO2), HCO(3) (-) and base excess of venous blood showed no detectable change during duodenal infusion of either acidic or alkaline solutions. Metabolic acidosis or alkalosis, therefore, cannot be considered to play any part in controlling gastric function. The results thus corroborate the notion that the receptors controlling gastric function are localized in the intestinal mucosa.8. Our results suggest that interplay between acid and osmolality of gastric chyme occurs in the rostral part of the duodenum to produce a graded inhibitory effect which by negative feedback modulates the gastric effectors that normally activate smooth muscle, parietal cells and zymogen cells.

1. Gastric emptying, gastric acid and pepsinogen secretion were assessed simultaneously in the conscious calf using the test meal and duodenal perfusion technique (Bell & Mostaghni, 1975).2. When 60 mM-HCl was infused into the duodenum, gastric emptying was arrested but both acid and pepsinogen secretion continued at a low level. Duodenal infusion with isotonic NaHCO(3) caused rapid exponential emptying of the test meal and acid and pepsinogen output was more than doubled.3. Duodenal infusion of amino acids in isotonic NaHCO(3) did not affect the rapid emptying, except infusion with tryptophan, which caused a measureable degree of inhibition of emptying, with concomitant effects on acid and pepsinogen secretion4. Tryptamine and 5-hydroxytryptamine (5-HT) incorporated in low concentration into isotonic NaHCO(3) also produced depression of gastric emptying, acid and pepsinogen levels comparable to the response initiated by acid infusate. Tryptophan was effective only in non-physiological amounts while 5-HT and tryptamine were active in smaller doses.5. Our results suggest that the inhibition of gastric emptying following duodenal infusion of tryptophan noted by Stephens, Woolson & Cooke (1975) may be due to the duodenal synthesis of its biogenic amine derivatives tryptamine and 5-HT.6. The level of activity of the three gastric functions, emptying, acid secretion and pepsinogen secretion appears to be linked. A single stimulus, therefore, could evoke a duodenal receptor or receptors to mediate or suppress activity of the gastric smooth muscle and secretory cells through interrelated mechanisms. The effect of some duodenal infusates, however, produces some variability in response which suggests differential activation of different receptors with consequent variable motor activity on effector cells.

1. The relative importance of energy content and osmolality of the duodenal chyme in the feed-back control of gastric emptying was investigated in the milk-fed calf fitted with gastric (abomasal) and duodenal re-entrant cannulae. 2. Duodenal infusion of isosmolal solutions, containing glucose, fructose or galactose, with a range of combustible energy content (0--1.46 MJ/l.) resulted in the same high rate of emptying of test meals from the stomach (abomasum). Abomasal emptying was, therefore, not affected by the energy content of the duodenal infusate. 3. Gastric secretion of acid and pepsinogen, and the volume of gastric secretions produced were also unaffected by the energy content of isosomolal duodenal infusates. 4. The results of the study show that the combustible energy content of the intestinal chyme is not a direct determinant of gastric function and that total osmolality of the lumenal contents is the only parameter influencing duodenal receptors under the conditions of our experiments.

Levels of endogenous somatostatin, gastric inhibitory polypeptide (GIP), glucagon and insulin were measured during gastric (abomasal) emptying in the conscious calf. Isotonic NaHCO3 infused into the duodenum increased rates of emptying of a saline test meal and of gastric acid secretion, but had no effect on basal levels of blood glucose, somatostatin, GIP, insulin or glucagon. By contrast, intraduodenal infusion of 60 mM-HCl caused complete inhibition of gastric emptying, reduction of acid secretion, and an immediate increase in plasma somatostatin from 121.3 +/- 9.4 (S.E.M.) to 286.3 +/- 16.3 pg/ml (P less 0.01) but levels of GIP, insulin, glucagon and glucose were unaltered. Intravenous injection of somatostatin (0.5 microgram/kg) suppressed the antral electromyographic recording and gastri efflux so long as plasma somatostatin levels remained above approx. 200pg/ml. This suggest that somatostatin can be released by intraduodenal acidification and that it inhibits gastric function by an endocrine effect. Since somatostatin retards gastric emptying it may therefore have an indirect role in nutrient homeostasis by limiting discharge of gastric chyme to the duodenum.

Preruminant (milk-fed) calves were prepared with an abomasal and re-entrant duodenal cannulae to assess the effect of acid test meals on abomasal emptying and secretion. Isotonic saline meals acidified with hydrochloric acid to pH 2 instilled directly into the abomasum did not affect abomasal emptying or acid and pepsin secretion when compared with saline meals at pH 6. Isotonic saline meals at pH 1.2 significantly inhibited abomasal acid secretion, but had little effect on emptying or pepsinogen secretion. Abomasal emptying, acid secretion and pepsinogen secretion were significantly inhibited when acid was introduced into the duodenum, irrespective of the acidity of the test meal. It is concluded that in the calf acid meals inhibit gastric acid secretion alone without effect on pepsinogen secretion and abomasal emptying. All three abomasal functions, however, were inhibited by acidification of the duodenum.

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.