Figure 401

Influences on parietal cell acid secretion. The pathways by which secretagogues are believed to stimulate hydrogen ion production and secretion are shown. In addition, the sites of action (broken arrows) of various acid suppressive medications are shown. A, atropine; PGE, prostaglandin E; H, histamine; G, gastrin, Riand Rs, inhibitory and stimulatory receptor-binding sites; Giand Gs, inhibitory and stimulatory catalytic subunits; ATP, adenosine triphosphate; ATPase, adenosine triphosphatase. (Reprinted with permission from Wolfe MM and Soll AH. The physiology of gastric acid secretion. N Engl J Med 1988;319:1707.)

secretion. Evidence from animal studies suggests that after protein amino acids are converted to amines, gas-trin is released.

Gastric acid secretion is inhibited in the presence of acid itself. A negative feedback occurs when the pH approaches 2.5 such that further secretion of gastrin is inhibited until the pH rises. Ingested carbohydrates and fat also inhibit acid secretion after they reach the intestines; several hormonal mediators for this effect have been proposed. The secretion of pepsinogen appears to parallel the secretion of H+, while the patterns of secretion of mucus and bicarbonate have not been well characterized.

The integrity of the mucosal lining of the stomach and proximal small bowel is in large part determined by the mucosal cytoprotection provided by mucus and bicarbonate secretion from the gastric and small bowel mucosa. Mucus retards diffusion of the H+ from the gastric lumen back into the gastric mucosal surface. In addition, the bicarbonate that is secreted into the layer between the mucus and epithelium permits a relatively high pH to be maintained in the region next to the mu-cosal surface. If any H+ does diffuse back to the level of the mucosal surface, both the local blood supply and the ability of the local cells to buffer this ion will ultimately determine whether peptic ulceration will occur. With duodenal and gastric peptic ulcer disease, a major causative cofactor is the presence of gastric Helicobacter pylori infection.

Medications that raise intragastric pH are used to treat peptic ulcer disease and gastroesophageal reflux disease. In addition, agents that enhance mucosal cyto-protection are used to decrease ulcer risk.

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