CorpusHuman Anatomy
DigestivePhysiological process

Gastric acid secretion and its phases

Also known as: cephalic phase, gastric phase, intestinal phase, HCl secretion

Acid secretion is driven by three stimulants that reinforce each other: acetylcholine, gastrin and histamine. It is braked by somatostatin, and it runs in cephalic, gastric and intestinal phases.

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Overview

Basal acid output≈2–5 mmol/h
Maximal acid output≈20–40 mmol/h
Phase contributionsCephalic ≈30% · gastric ≈60% · intestinal ≈5–10%

Basal (interdigestive) acid output is modest, about 2–5 mmol/h, and follows a circadian rhythm with a night-time peak. Maximal stimulated output reaches about 20–40 mmol/h.

Stimulation converges on the parietal cell. ACh from the vagus acts directly on M3 receptors and also releases gastrin (via GRP) and histamine. Gastrin from antral G cells acts mainly by releasing histamine from ECL cells. Histamine acts on H2 receptors. Their combined effect is greater than the sum of their separate effects (potentiation).

Inhibition: when antral pH falls below about 3, D cells release somatostatin, which suppresses G cells, ECL cells and parietal cells. This is the main negative-feedback loop. Prostaglandins (PGE₂) and enterogastrones from the duodenum (secretin, GIP, CCK, PYY, GLP-1) also inhibit secretion.

Parts & subdivisions

  1. Cephalic phase (≈30%)
    Sight, smell, taste, thought of food and chewing drive vagal output. ACh acts on parietal and chief cells, and GRP releases gastrin. Vagotomy abolishes this phase. Hypoglycaemia stimulates it, which was the basis of the old insulin "sham feeding" test.
  2. Gastric phase (≈60%)
    Distension activates vagovagal and local enteric reflexes. Peptides and amino acids (especially phenylalanine and tryptophan), caffeine, calcium and alcohol stimulate G cells. Food buffers acid, which removes the somatostatin brake.
  3. Intestinal phase (≈5–10%)
    Briefly stimulatory (duodenal gastrin, absorbed amino acids), then mostly inhibitory. Acid, fat and hyperosmolar chyme in the duodenum trigger the enterogastric reflex and release enterogastrones, which reduce acid secretion and gastric emptying.
  4. Mucosal defence
    Adherent mucus–bicarbonate gel, tight junctions, rapid epithelial restitution, high mucosal blood flow and prostaglandins. These protect the stomach from its own acid and pepsin.

Function

  • Matches acid and pepsin output to the protein load and buffering capacity of the meal.
  • Protects the duodenum by feedback inhibition of acid secretion.
Regulation

Stimulants: ACh (M3), gastrin (CCK2), histamine (H2). Inhibitors: somatostatin, PGE₂, secretin, GIP, CCK and other enterogastrones.

Clinical significance

H. pylori and acid

Antral-predominant infection reduces D cells, so gastrin and acid rise and duodenal ulcers form. Body-predominant (pangastritis) infection causes atrophy and low acid output, leading to gastric ulcer and gastric cancer.

NSAIDs

By inhibiting COX-1 they cut PGE₂. Mucus and bicarbonate secretion and mucosal blood flow fall and acid secretion is less restrained, so ulcers form even with normal acid output.

Zollinger–Ellison syndrome

Autonomous gastrin secretion by a gastrinoma raises basal acid output to very high levels (often over 15 mmol/h). Fasting gastrin is high despite a low gastric pH. Treatment is high-dose PPIs and resection.

Test yourself

Which phase of gastric secretion accounts for most of the acid secreted in response to a meal?
  1. Cephalic phase
  2. Gastric phase
  3. Intestinal phase
  4. Interdigestive phase

Answer: Gastric phase

The gastric phase provides about 60% of acid output, driven by distension (vagovagal and local reflexes) and by peptides and amino acids stimulating gastrin release. The cephalic phase provides about 30% and the intestinal phase about 5–10%; the intestinal phase is mostly inhibitory.

More digestive system questions

Compiled from standard anatomy and physiology references — see the Digestive System sources. For education only; not medical advice.