Study guide
Study guide

Gastric secretions

Describe the formation of gastric acid and the regulation of gastric acid secretion

Approximately 2 L/day of gastric secretions are produced:

  • Hydrogen ion concentration: ~150 mmol/L
  • Chloride concentration: ~180 mmol/L
  • Maintains an intragastric pH of 1.0–1.5

Mechanism

  1. CO₂ and H₂O are present within parietal cells.
    • Carbonic anhydrase catalyses: CO2+H2O→HCO3−+H+ \text{CO}_2 + \text{H}_2\text{O} \rightarrow \text{HCO}_3^- + \text{H}^+
  2. Apical membrane
    • H⁺/K⁺-ATPase (proton pump) actively secretes H⁺ into the gastric lumen in exchange for K⁺.
    • K⁺ is recycled back to the lumen via apical potassium channels.
  3. Basolateral membrane
    • HCO₃⁻/Cl⁻ exchanger transports bicarbonate into the blood in exchange for chloride.
  4. Chloride
    • Diffuses into the gastric lumen along its concentration gradient via apical Cl⁻ channels.
  • Net effects
    • Formation of HCl in the gastric lumen
    • Entry of HCO₃⁻ into the bloodstream, causing a short-lived post-prandial metabolic alkalosis known as the alkaline tide

Regulation

Phase

Events

Cephalic phase

30% of total gastric secretions.

Triggered by sight, smell, taste, and anticipation of food.

Mediated by the vagus nerve:

  • Acetylcholine stimulates M3 receptors on parietal cells → ↑ acid secretion
  • ↑ Gastrin-releasing peptide (GRP) secretion which stimulates gastrin release from G cells
  • Vagal inhibition of somatostatin → disinhibition of G and parietal cells

Gastric phase

60% of total gastric secretions.

Gastric distension stimulates gastrin release from G cells:

  • Directly stimulates parietal cells via gastrin receptors.
  • Indirectly stimulates acid secretion by increasing histamine release from enterochromaffin-like (ECL) cells, acting on parietal H₂ receptors to increase acid secretion.

Amino acids and peptides also directly stimulate parietal cell activity.

Intestinal phase

~10% of total gastric secretions.

Triggered by chyme entering the duodenum.

Initially may weakly stimulate gastric acid secretion.

Subsequently inhibited by:

  • Secretin → directly inhibits gastric acid secretion
  • Gastric inhibitory polypeptide (GIP) → stimulates somatostatin release → inhibits parietal cells

Describe the functions of the gastric secretions

The stomach is capable of much more than the secretion of gastric acid. However these additional functions appear to be of much less interest to college examiners.

Secretion

Cell Type

Effect

Gastric acid (HCl)

Parietal cells

  • Has intrinsic proteolytic activity.
  • Produces the acidic environment required to converts pepsinogen to the active pepsin, a key proteolytic enzyme.
  • Gastric acid is bactericidal.
  • Facilitates conversion of Fe³⁺ to Fe²⁺, which is more easily absorbed.

Gastrin

G cells

  • Stimulates gastric acid and pepsin secretion.
  • Trophic effects on gastric mucosa.

Electrolytes

Parietal and epithelial cells

Parietal cells secrete H⁺, Cl⁻, K⁺.

Other epithelial cells secrete Na⁺, K⁺, Cl⁻, HCO₃⁻.

Electrolyte secretion maintains gastric fluid composition and supports acid secretion and mucosal buffering.

Pepsinogen

Chief cells

An inactive zymogen which is converted to pepsin in the acidic gastric environment.

Pepsin is a key proteolytic enzyme involved in the digestion of proteins.

Intrinsic factor

Parietal cell

Binds vitamin B12, enabling its absorption in the terminal ileum.

Mucous & bicarbonate

Mucous cells

  • Forms protective mucous barrier.
  • Buffers acid at epithelial surface, protecting the gastric mucosa.

Prostaglandins

Various cells

  • Increases mucous and bicarbonate secretion.
  • Maintains mucosal blood flow.
  • Inhibits excessive acid secretion.
A bad mnemonic - PIMPAGE
  • Pepsinogen
  • Intrinsic factor
  • Mucous + bicarbonate
  • Prostaglandins
  • Acid
  • Gastrin
  • Electrolytes
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