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Bicarbonate secretion from the surface epithelial cells in the duodenum is an active process depending on tissue metabolism and blood flow, and regulated by humoral and neuronal factors as well as endogenous prostaglandins (PGs). The duodenal mucosa has been also able to respond luminal acid by a significant rise in alkaline secretion, mediated mainly by PGs, and the impairment of this process is involved in the pathogenic mechanism of various duodenal ulcer models. The mechanism of mucosal protection by HCO3- secretion is two ways: one is neutralization of luminal acid, and the other the establishment of pH gradient in the mucus gel with the aid of the physicochemical property of mucus. Although the majority of H+ is neutralized by secreted HCO3- in the lumen and mucus gel, the ultimate mucosal protection is ensured by removal of back-diffused H+ through intramucosal neutralization with HCO3- and translocation by blood flow. Thus, HCO3- secretion in collaboration with mucus plays an important role as the first line of defense (pre-epithelial barrier) in the duodenal mucosal protection.

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Bicarbonate Secretion in the Mucosal Defensive Mechanism of the Duodenum. Acid Neutralization with HCO&lt;SUB&gt;3&lt;/SUB&gt;&lt;SUP&gt;-&lt;/SUP&gt; in the Lumen and Mucus Gel