REVIEW ARTICLE - GASTRODUODENAL BICARBONATE SECRETION

The gastroduodenal epithelium is covered by an adherent mucus layer in to which bicarbonate is secreted by surface epithelial cells. This muc us-bicarbonate barrier is an important first line of defence against d amage by gastric acid and pepsin, and has been demonstrated in all spe cies including human. Similar to gastric acid secretion, regulation of gastric and duodenal bicarbonate secretion can be divided into three phases: cephalic, gastric and duodenal. In humans, sham-feeding increa ses bicarbonate secretion in both the stomach and duodenum which is me diated by cholinergic vagal fibres in the stomach, but seems to be non cholinergic in the duodenum. Gastric distention and luminal acidificat ion increases gastric bicarbonate production. Whereas there are no dat a relating to the gastric phase of human duodenal bicarbonate secretio n, in animals, food and acid in the stomach independently stimulate du odenal bicarbonate output. To date, the duodenal phase of human gastri c bicarbonate secretion has not been studied, but data from animals re veal that duodenal acidification augments bicarbonate secretion in the stomach. In all species tested, direct acidification of the duodenum is a potent stimulant of local bicarbonate production. In humans, the pH threshold for bicarbonate secretion is pH 3.0. Mediation of gastrod uodenal bicarbonate secretion is provided by a variety of agonists and antagonists, tested mainly in animals, but some have been evaluated i n humans. Prostaglandins of the E class and VIP are major factors that control bicarbonate secretion. Bicarbonate secretion, and the mucus-b icarbonate layer in general, is adversely effected by ulcerogenic fact ors such as aspirin, NSAIDs, bile salts, and cigarette smoking. Furthe rmore, duodenal ulcer patients have an impairment in bicarbonate produ ction within the duodenal bulb, at rest and in response to stimulation . These findings indicate that the mucus-bicarbonate barrier is an imp ortant first line of defence in the pathogenesis of peptic ulcer disea se.