This study examines the effect of graded
antral distension with
acid (0.1 M HCl) or
alkali (0.1 M NaHCO3) on
pentagastrin-stimulated
acid secretion in two groups of dogs. Group A consisted of six dogs provided with innervated
antral pouch. In these dogs, the vagal branches to the fundus, as well as the extragastric vagal divisions (hepatic and celiac), were preserved. All of these animals had a
gastric fistula in the main stomach, and in two a denervated fundic pouch or Heidenhain pouch was constructed in addition. Group B consisted of four dogs with an innervated
antral pouch and
gastric fistula. In this latter group, however,
parietal cell vagotomy as well as extragastric
vagotomy (division of the hepatic and celiac branches) was performed so that the only vagal communication was between the antrum and the CNS.
Antral distension with
acid caused significant inhibition of
pentagastrin-stimulated
acid secretion from both the
gastric fistula and the Heidenhain pouch in Group A dogs.
Antral acidification without distension did not inhibit. Alkaline
antral distension in this group caused much less inhibition of
acid secretion, but did cause significant increase in circulating immunoreactive
gastrin. In Group B dogs,
antral distension with neither
acid nor
alkali caused inhibition of
pentagastrin-stimulated
acid secretion, indicating that intact vagal supply to the oxyntic mucosa and/or to the extragastric abdominal organs is necessary for the inhibitory mechanism to operate. The results of this study suggest that: a)
antral acidification per se does not inhibit
pentagastrin-stimulated
acid secretion; and b)
antral distension with
acid, and to a lesser extent with
alkali, is inhibitory only if vagal innervation to the fundus and other abdominal viscera is preserved. The observations are compatible with the hypothesis that
antral distension activates a neurohumoral inhibitory mechanism releasing the inhibitor reflexly from sites other than the antrum or CNS.