Gastric Emptying

Gastric juice production

Production of gastric juice
FIGURE 1 - Production of gastric
juice (click to enlarge)
The production of gastric juice occurs in three overlapping phases (Figure 1).

The steps in the diagram are explained in the text below.

Cephalic (‘head’) phase – Initiated by the thought, sight, smell and taste of food. The vagus nerve is stimulated, causing the release of gastrin, acetylcholine and histamine, which interact with receptors on the parietal cells to produce HCl.

Gastric (‘belly’) phase – Accounts for ~80% of gastric acid production. Protein fragments, stomach distension and stimulants (alcohol and caffeine) stimulate the vagal nerve in the stomach wall, activating release of acetylcholine, which causes production of acid in parietal cells. Acetylcholine also stimulates gastrin release, which in turn stimulates parietal cells to increase acid secretion. Peptides present in the stomach also directly stimulate gastrin release. Proteins in food buffer the acid, therefore, more gastrin, and hence acid, is released to keep stomach pH acidic.

Intestinal phase – Peptides in the duodenum stimulate the production of intestinal gastrin to secrete gastric juice (excitatory phase).

Gastrin – Reacts with gastrin receptors on parietal cells in the gastric glands of the stomach to stimulate production of HCl.

Acetylcholine – Reacts with muscarinic M3-receptors on parietal cells in the gastric glands of the stomach to stimulate production of HCl.

Histamine – Reacts with histamine H2-receptors on parietal cells in the gastric glands of the stomach to stimulate production of HCl.

Acid secretion – HCl is produced in parietal cells in the gastric glands of the stomach wall and released into the stomach.

Gastric emptying – The movement of digested chyme from the stomach to the duodenum through the pyloric sphincter is monitored by factors in the duodenum, stomach, and central nervous system. The more distended the stomach, the stronger the force exerted on the pyloric sphincter.

Gastric emptying is also stimulated by the presence of partially digested proteins and stimulants (eg, caffeine and alcohol). Distension of the stomach stimulates the vagus nerve to strengthen the peristaltic waves and increase gastrin production, increasing gastric juice production and stimulating stomach motility. The pyloric sphincter then relaxes to allow the chyme to pass through it and into the duodenum.

CCK, secretin, GIP – Enterogastrones that are released when acid chyme enters the duodenum. They inhibit the production of HCl from the parietal cells and pepsinogen from the chief cells, and inhibit gastric emptying.

Acid chyme in the duodenum stimulates release of enterogastrones – cholecystokinin (CCK), secretin and gastric inhibitory peptide (GIP), which inhibit the production of HCl from the parietal cells and pepsinogen from the chief cells, thus inhibiting gastric emptying.

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