Pyloro-oxyntic neurohumoral inhibitory reflex of acid secretion

Abstract

Antral distension has previously been shown to activate a neurohumoral mechanism that inhibits acid secretion from the main stomach and from a denervated fundic pouch. Neither the antrum nor the central nervous system (CNS) appears to be the source of the inhibitory substance since, when only vagal communication between the antrum and the CNS is maintained, with vagal denervation of all other abdominal organs, antral distension no longer causes inhibition of acid secretion. The present study was designed to investigate whether intact vagal innervation to the oxyntic cell mucosa was a necessary pathway for this inhibitory mechanism. In four dogs with innervated antral pouch (AP) and gastric fistula (GF), the effect of antral distension with 0.1 M HCl at 40-cm pressure on a plateau of GF acid secretion in response to pentagastrin (4.0 μg kg −1 hr −1) was studied before and after proximal gastric vagotomy (PGV). The completeness of vagal denervation of the proximal stomach was shown by failure of acid response to insulin hypoglycemia after PGV. Prior to PGV, antral distension caused a significant inhibition of GF acid response to pentagastrin, with a maximal inhibition of 55% of the plateau of acid secretion. After PGV, antral distension was without inhibitory effect. These results indicate that the inhibitory action of antral distension is mediated by a pyloro-oxyntic reflex. Further, since antral distension inhibits a denervated pouch, the study suggests that this pyloro-oxyntic reflex might release a humoral inhibitor from the oxyntic mucosa.