Intragastric CO2 and nitric oxide participate in the regulation of peptone-induced gastrin release in humans

Background: Moderate acidification of the gastric lumen inhibits peptone-in duced gastrin release. The aim of the present study was to investigate if t he gastric acid neutralization products CO2 (from secreted HCO3-) and NO (f rom reduced salivary nitrite) could act as intermediate messengers between luminal acidity and the inhibition of peptone-induced,gastrin release. Meth ods: Fourteen healthy volunteers (mean age, 27 years; range, 20-39 years; 3 women) participated in the study. Intragastric perfusion with saline or pe ptone was performed on the healthy volunteers. Venous blood samples were an alyzed for serum gastrin concentrations. Intragastric NO was measured by ch emiluminescence. Results: Basal serum gastrin ranged between 11 and 23 pmol /l. Peptone in Sorensen's phosphated buffer (pH 6.9, P-CO2 0 mmHg) increase d serum gastrin by 83% +/- 23%, whereas acidified peptone (pH 2.0) did not stimulate gastrin release. Acidified peptone buffered with NaHCO3 to neutra lity (pH 6.9, P-CO2 approximately 600 mmHg) increased serum gastrin by 166% +/- 29%. Low intragastric NO levels were obtained by deviation of saliva. During such salivary depletion, acidified peptone (pH 2.0) stimulated gastr in release to a level of about 40% of the control response (pH 6.9). This p eptone-induced gastrin response during salivary deviation was inhibited by addition of nitrite to the perfusate. Conclusions: Acid-induced inhibition of peptone stimulated gastrin release is partly dependent on intraluminal N O fanned in the reaction between salivary nitrite and gastric acid. In addi tion, the gastric acid neutralization product CO2 seems to potentiate the e ffect of peptone on gastrin release.