The interplay between hydrogen ions, bicarbonate ions and osmolarity in the anterior duodenum modulating gastric function in the conscious calf

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Abstract
Gastric emptying, gastric acid and pepsinogen secretion were assessed simultaneously in the conscious calf using the test meal and duodenal perfusion technique (Bell et Mostaghni, 1975). Duodenal infusion of NaCl at a constant osmolality of 300 mosmol/kg, but with pH ranging from 2.0-12.0, did not alter the high level of gastric emptying and secretion already reported for isotonic NaCl or NaHCO3 alone (Bell et Mostaghni, 1975; Bel et Webber, 1979). Gastric function is unaffected by gastric chyme at pH 2.0-12.0 entering the duodenum, or isotonicity is dominant over pH in activating duodenal receptors which increase motor activity. When the pH of the isotonic NaCl was reduced by the addition of HCl to < 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. When the same amount of acid but at differing concentrations and infusion rates was introduced into the duodenum uniform inhibition of gastric function occurred. Duodenal acid receptors probably respond to acid concentration and flow rate to produce an integrated response in proportion to the amount (concentration X volume) of acid present. Isotonic NaHCO3 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 NaHCO3 at high pH is probably due to CO32-, since Na2CO3 and LI2CO3, but not LiCl, produce a similar inhibitory effect on gastric function. The inhibitory effect of CO32- gives some support to the existence of a CO2-sensor as suggested by Hunt et Knox (1972), whereby increased PCO [partial pressure of CO2] produced by intracellular or intercellular neutralization of CO32- by duodenal H+ activates acid receptors. Simultaneous perfusion of HCl and excess NaHCO3 produced a rise in intraluminal PCO2,, but did not inhibit gastric function, which is contrary to the idea of a direct intraluminal effect of CO2 on duodenal receptors. The pH, PO2, PCO2, HCO3- and base excess of venous blood showed no detectable change during duodenal infusion of either acidic or alkaline solutions. Metabolic acidosis or alkalosis, cannot be considered to play any part in controlling gastric function. The results corroborate the notion that the receptors controlling gastric function are localized in the intestinal mucosa. Probably 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.