Gastroduodenal mucosal secretion of bicarbonate and mucus. Physiologic control and stimulation by prostaglandins.
Bicarbonate secretion by the surface epithelium in the stomach and duodenum maintains a nearly neutral pH in the mucus gel adherent to the surface despite acidities as high as pH 2.0 to 3.0 in the gastric lumen and pH 1.5 to 2.0 in the duodenal lumen. This strongly suggests that the alkaline secretion, together with the mucus gel, provides a first-line of protection in the stomach, and this may be the main mechanism of defense in the duodenum. Bicarbonate secretion is increased by physiologic stimuli such as sham-feeding or the presence of acid in the lumen. Endogenous mucosal production of prostaglandins is important in mediating the response to the latter. Administration of E-type prostaglandins stimulates alkaline secretion in both the stomach and duodenum and also increases the thickness of the mucus layer adherent to the mucosa. The consequent increase in surface alkalinity most likely potentiates the mucosal resistance to luminal acid and pepsin.
Flemström
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D015064:16,16-Dimethylprostaglandin E2 / Q000494:pharmacology; D000818:Animals; D001639:Bicarbonates / Q000378:metabolism*; D015232:Dinoprostone; D004386:Duodenum; D005753:Gastric Mucosa / Q000187:drug effects / Q000378:metabolism*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D007413:Intestinal Mucosa / Q000187:drug effects / Q000378:metabolism*; D009093:Mucus / Q000378:metabolism*; D010295:Parietal Cells, Gastric / Q000378:metabolism; D011453:Prostaglandins / Q000502:physiology*; D011458:Prostaglandins E / Q000494:pharmacology; D051381:Rats
D001639:Bicarbonates; D011453:Prostaglandins; D011458:Prostaglandins E; D015232:Dinoprostone; D015064:16,16-Dimethylprostaglandin E2