Overview
This lecture explains the mechanisms and regulation of gastric secretions during the cephalic and gastric phases, detailing the roles of various stimuli, cells, and neurotransmitters in acid and enzyme production.
Phases of Gastric Secretion
- Gastric secretion occurs in three phases: cephalic, gastric, and intestinal.
- Cephalic phase accounts for about 1/3 of gastric juice secretion; gastric phase accounts for about 2/3.
- Cephalic phase is triggered before food enters the stomach; gastric phase is triggered when food is present in the stomach.
Cephalic Phase
- Stimuli: sight, thought, smell, and taste of food activate the brain (cerebral cortex, hypothalamus, medulla).
- Vagus nerve mediates signals from the brain to the stomach, stimulating parietal and chief cells.
- Parietal cells secrete hydrochloric acid (HCl); chief cells secrete pepsinogen.
- Sympathetic nervous system inhibits gastric secretion (e.g., during stress).
Gastric Phase
- Triggered by stomach distension (stretch) and presence of partially digested proteins.
- Distension activates stretch receptors, initiating vago-vagal and local (enteric) reflexes.
- G cells in the antrum secrete gastrin in response to proteins, stimulating parietal and chief cells.
- Gastrin acts on parietal cells to increase HCl (via CCK2 receptors) and on chief cells to increase pepsinogen secretion.
Regulation of Secretion
- Low pH (high H+) in the stomach triggers D cells to release somatostatin, which inhibits G cells and parietal cells, reducing gastrin and acid secretion.
- Vagus nerve (via acetylcholine) stimulates gastric cells and inhibits D cells.
- Histamine from ECL cells further stimulates acid secretion via H2 receptors on parietal and chief cells.
- Prostaglandin E2 (PGE2) inhibits acid secretion via EP-3 receptors on parietal cells.
Mechanism of Acid & Enzyme Production
- Parietal cells produce HCl via CO2 + H2O → H2CO3 (carbonic anhydrase); H2CO3 dissociates to H+ and HCO3–.
- H+ secreted into the lumen by proton-potassium pump; HCO3– enters blood, causing “alkaline tide.”
- Chief cells release pepsinogen, converted to pepsin by acidic pH (optimal 1.8–3.5).
Mucosal Barrier Protection
- Mucosal barrier, formed by foveolar and mucus neck cells, protects stomach lining.
- Barrier contains water, electrolytes, phospholipids, mucin proteins, and bicarbonate.
Key Terms & Definitions
- Cephalic Phase — Gastric secretion initiated by sensory input before food enters the stomach.
- Gastric Phase — Secretion phase stimulated by food in the stomach.
- Parietal Cell — Stomach cell that secretes hydrochloric acid and intrinsic factor.
- Chief Cell — Stomach cell that secretes pepsinogen.
- G Cell — Antral cell that secretes gastrin hormone.
- D Cell — Cell releasing somatostatin, inhibiting acid and gastrin secretion.
- ECL Cell — Enterochromaffin-like cell releasing histamine to stimulate acid secretion.
- Gastrin — Hormone stimulating acid and pepsinogen release.
- Somatostatin — Hormone inhibiting gastric acid and gastrin release.
- Alkaline Tide — Temporary rise in blood pH due to bicarbonate release during acid secretion.
- Mucosal Barrier — Protective layer preventing stomach self-digestion.
- Vago-vagal Reflex — Neural loop involving afferent and efferent vagus nerve signaling in the stomach.
Action Items / Next Steps
- Review details of the intestinal phase and mucosal barrier in the next lecture or assigned reading.