Gastric mucus, a viscous gel that coats the entire gastric mucosa, is produced by and secreted from the surface epithelial cells. Although 95% water by weight, gel mucus is a polymer of four equal-sized subunits joined by disulfide bridges. Carbohydrate side chains include N-acetylglucosamine, N-acetylgalactosamine, galactose, fucose, neuraminic acid, and sialic acid. At a concentration of about 20 mg/ml, the viscosity begins to rise, and a gel is formed. The thickness of the gel mucus layer is dynamic, and a function of release from surface epithelial cells and mechanical and proteolytic degradation within the lumen. An increase in luminal fluid glycoprotein output has been observed in response to splanchnic and vagal nerve stimulation, topical acetylcholine, prostaglandins, carbenoxolone, and parenteral secretin. Topical prostaglandins and carbenoxolone have been observed to increase mucus gel thickness. Gastric bicarbonate secretion is also thought to be a function of the surface epithelial cell. The magnitude of stimulated gastric bicarbonate secretion is 5 to 10% of maximal acid secretion for a given surface area of mucosa. Stimulants of gastric bicarbonate secretion are carbachol, Ca++, c-GMP, 16-16 dimethyl PGE2, and PGF2 alpha. Inhibitors of gastric bicarbonate secretion include atropine, metabolic inhibitors, acetazolamide, alpha-adrenergic agents, and inhibitors of prostaglandin synthesis. Taken together, these observations lend credence to the hypothesis that an unstirred layer of mucus, rich in bicarbonate, may offer significant protection against acid-peptic mucosal injury by neutralizing luminal acid and thereby providing the apical membrane of the surface epithelial cell with a near neutral pH milieu.