Phases of Gastric Secretion

Mnemonic

Three phases, named for where the stimulus is:

• Cephalic, about 30 per cent - sight, smell, taste and thought of food, mediated by the vagus and acetylcholine. This is the phase abolished by vagotomy
• Gastric, about 60 per cent - distension and peptides in the stomach, mediated by gastrin from antral G cells. The largest contributor
• Intestinal, about 10 per cent - initially stimulatory, then inhibitory as acid, fat and hyperosmolar chyme reach the duodenum, mediated by secretin, CCK and GIP (the enterogastric reflex)

“Think, distend, then switch off.”

Acid secretion at the parietal cell is driven by three receptors, all converging on the H+/K+ ATPase proton pump: muscarinic M3 (acetylcholine), gastrin (CCK-B) and histamine H2. Histamine from ECL cells is the final common amplifier, which is why H2 blockers work at all and why proton pump inhibitors, acting on the pump itself, work better than either.

Expansion

• Cephalic phase (about 30 per cent) - sight, smell, taste and thought of food. Entirely vagal, acting directly on parietal cells and by releasing gastrin. Demonstrated by sham feeding
• Gastric phase (about 60 per cent) - food in the stomach. Distension triggers vagovagal reflexes, and peptides and amino acids stimulate G cells to release gastrin
• Intestinal phase (about 10 per cent) - initially stimulatory as protein enters the duodenum, then predominantly inhibitory

Inhibition comes from:

• Acid in the antrum (pH under 3) suppressing gastrin, through somatostatin from D cells
• Acid in the duodenum releasing secretin
• Fat and hypertonicity in the duodenum releasing cholecystokinin and GIP, and triggering the enterogastric reflex

This layered control explains why the historical operations for ulcer disease targeted the vagus (cephalic phase) or the antrum (gastric phase), and why modern acid suppression targets the final common pathway instead.