Overview
This lecture explains the cephalic and gastric phases of gastric secretions, focusing on stimulation, inhibition, and the cellular mechanisms of acid and enzyme release in the stomach.
Phases of Gastric Secretion
- Gastric secretion occurs in three phases: cephalic, gastric, and intestinal.
- Cephalic phase accounts for about 1/3 of gastric juice production and is triggered before food enters the stomach.
- Gastric phase accounts for about 2/3 of gastric juice production and occurs when food is in the stomach.
Cephalic Phase
- Stimuli: sight, smell, thought, and taste of food activate the cerebral cortex.
- Cerebral cortex signals the hypothalamus, then the medulla, and finally the dorsal nucleus of the vagus nerve.
- Vagus nerve stimulates parietal cells (HCl) and chief cells (pepsinogen) in the stomach.
- Cephalic phase secretion occurs before food is present in the stomach.
- Sympathetic nervous system activation (stress, emotions) inhibits cephalic phase via splanchnic nerves.
Gastric Phase
- Triggered by stomach distension (stretch) and presence of partially digested proteins.
- Distension activates stretch receptors, leading to a vago-vagal reflex (long arc) and local enteric (short arc) reflexes.
- G cells (in antrum) detect proteins and release gastrin hormone.
- Gastrin stimulates parietal cells (HCl) and chief cells (pepsinogen).
- Gastric phase is inhibited by sympathetic activation and somatostatin (from D cells), which responds to high proton (low pH) levels.
Cellular Mechanisms of Secretion
- Parietal cells produce HCl via the proton-potassium ATPase ("proton pump") using CO₂ and water.
- Bicarbonate produced exits into blood, creating the "alkaline tide."
- Chloride ions enter to balance charge and are secreted with H⁺, forming HCl.
- Chief cells release pepsinogen, which is converted to active pepsin at low pH (1.8–3.5).
Regulation of Gastric Secretions
- Stimulation: acetylcholine (M3 receptor), histamine (H2 receptor), and gastrin (CCK2 receptor) increase HCl and pepsinogen secretion.
- Inhibition: somatostatin (SST receptor) and prostaglandins (EP3 receptor) reduce secretion.
- Mucosal barrier (foveolar and mucus neck cells) protects stomach lining with mucus, mucins, water, phospholipids, electrolytes, and bicarbonate.
Key Terms & Definitions
- Cephalic phase — Gastric secretion phase triggered by sensory experiences before food enters the stomach.
- Gastric phase — Gastric secretion phase triggered by food being present and digested in the stomach.
- Parietal cell — Stomach cell producing hydrochloric acid (HCl) and intrinsic factor.
- Chief cell — Stomach cell producing pepsinogen, the precursor of pepsin.
- G cell — Antral enteroendocrine cell releasing gastrin.
- D cell — Cell releasing somatostatin, an inhibitor of gastric secretion.
- Vagus nerve — Parasympathetic nerve stimulating gastric secretions.
- Histamine — Paracrine stimulant of acid secretion via H2 receptors.
- Somatostatin — Hormone inhibiting gastric secretion in response to low pH.
- Alkaline tide — Alkalinity of blood leaving the stomach post-HCl secretion.
- Mucosal barrier — Protective mucus layer preventing damage from acid and pepsin.
Action Items / Next Steps
- Review the intestinal phase of gastric secretion in the next video.
- Study diagrams showing gastric gland cells and their regulation.