Gastric secretion.

This article summarizes data published during the past year that improve our understanding of the mechanisms by which various neurotransmitters, paracrine agents, and hormones regulate gastric acid secretion and are themselves regulated. The main stimulants of acid secretion are histamine, gastrin, and acetylcholine. The main inhibitor is somatostatin, which exerts a tonic restraint on parietal, enterochromaffin-like (ECL), and gastrin cells. Histamine, released from ECL cells, stimulates the parietal cell directly via H(2) receptors and indirectly via H(3) receptors coupled to inhibition of somatostatin secretion. Gastrin, acting via gastrin/cholecystokinin-B (CCK-B), now termed CCK(2), receptors on ECL cells activates histidine decarboxylase, releases histamine, and induces ECL hypertrophy and hyperplasia. The latter might be responsible for the rebound hyperacidity observed after withdrawal of long-term antisecretory therapy. The neurotransmitter pituitary adenylate cyclase-activating polypeptide stimulates histamine secretion from isolated ECL cells, but its physiologic role, if any, is not known. Acetylcholine, released from gastric postganglionic intramural neurons, stimulates the parietal cell directly via muscarinic M(3) receptors and indirectly by inhibiting somatostatin secretion. Although infection with H. pylori is associated with increased basal and stimulated acid outputs in patients with duodenal ulcer, most people infected with the organism are asymptomatic and have pangastritis with decreased acid output. In the latter, eradication of the bacterium leads to an increase in gastric acidity and is associated with a two-to threefold increase in gastroesophageal reflux.