H. pylori acutely inhibits gastric secretion by activating CGRP sensory neurons coupled to stimulation of somatostatin and inhibition of histamine secretion.

Acute Helicobacter pylori infection produces hypochlorhydria. The decrease in acid facilitates survival of the bacterium and its colonization of the stomach. The present study was designed to identify the pathways in oxyntic mucosa by which acute H.

Adrenomedullin stimulates somatostatin and thus inhibits histamine and acid secretion in the fundus of the stomach.

Adrenomedullin has recently been localized to enterochromaffin-like (ECL) and chief cells in the gastric fundus. It has been proposed that adrenomedullin may play a role in gastric mucosal defense and repair. In the present study, we have used the isolated, luminally perfused mouse stomach and superfused rat fundic segments to examine the effect of adrenomedullin on exocrine and endocrine secretion in this region of the stomach.

Regulation of atrial natriuretic peptide secretion by cholinergic and PACAP neurons of the gastric antrum.

Atrial natriuretic peptide (ANP) released from enterochromaffin cells helps regulate antral somatostatin secretion, but the mechanisms regulating ANP secretion are not known. We superfused rat antral segments with selective neural agonists/antagonists to identify the neural pathways regulating ANP secretion. The nicotinic agonist 1,1-dimethyl-4-phenylpiperazinium (DMPP) stimulated ANP secretion; the effect was abolished by hexamethonium but doubled by atropine.

Amylin, released from the gastric fundus, stimulates somatostatin and thus inhibits histamine and acid secretion in mice.

Background & Aims: Amylin, a peptide that displays 50% homology with calcitonin gene-related peptide (CGRP), is colocalized with somatostatin in endocrine cells of the gastric fundus. The present study was designed to determine the mechanism of action of amylin on gastric exocrine and endocrine secretion.

Methods: Acid secretion was measured in the isolated mouse stomach by titration.