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Gastric Secretion Phases

Sep 2, 2025

Overview

This lecture covers the mechanisms and regulation of gastric secretions, focusing specifically on the cephalic and gastric phases of digestion.

Phases of Gastric Secretion

  • Gastric secretion occurs in three phases: cephalic, gastric, and intestinal.
  • The cephalic phase accounts for about one-third of gastric juice production and occurs before food enters the stomach.
  • The gastric phase is responsible for about two-thirds of gastric secretion and begins when food enters/stretches the stomach.

Cephalic Phase: Stimulation & Inhibition

  • Stimulatory stimuli: sight, thought, smell, and taste of food activate the cerebral cortex.
  • Signals travel from the cortex to the hypothalamus, then medulla, and down the vagus nerve to the stomach.
  • Vagus nerve stimulates parietal cells (acid), chief cells (pepsinogen), and mucus secretion.
  • Inhibition occurs via sympathetic nervous system activation (e.g., stress), which suppresses vagal stimulation and secretion.

Gastric Phase: Stimulation & Inhibition

  • Initiated by stomach distension (stretch receptors) and the presence of partially digested proteins.
  • Stretch receptors trigger vago-vagal reflexes (long arc) and enteric (short arc) reflexes to stimulate secretion.
  • Proteins stimulate G cells in the antrum to release gastrin, which increases acid and pepsinogen secretion.
  • Sympathetic activation inhibits secretion; somatostatin (from D cells) is released in response to low pH and inhibits G cells (gastrin release).

Cellular & Molecular Mechanisms

  • Parietal cells produce HCl via carbonic anhydrase, generating protons and bicarbonate (alkaline tide in venous blood).
  • Gastrin stimulates parietal cells (via CCK-2 receptors) and chief cells (via CCK-1 receptors).
  • Acetylcholine stimulates secretion via muscarinic M3 receptors.
  • Histamine from ECL cells acts on H2 receptors to stimulate secretion.
  • Prostaglandins (PGE2) inhibit acid secretion via EP3 receptors.
  • Somatostatin acts through SST receptors to inhibit secretion.

Protective Mechanisms

  • Mucosal barrier (formed by foveolar and mucus neck cells) is composed of water, mucin proteins, bicarbonate, phospholipids, and electrolytes.
  • This barrier protects stomach lining from acidic and enzymatic damage.

Key Terms & Definitions

  • Cephalic Phase — pre-digestive phase, triggered by sensory stimuli before food enters the stomach.
  • Gastric Phase — begins when food enters the stomach, driven by stretch and chemical presence.
  • Parietal Cells — stomach cells that secrete hydrochloric acid (HCl).
  • Chief Cells — cells that secrete pepsinogen, the precursor of pepsin.
  • G Cells — enteroendocrine cells that release gastrin hormone.
  • D Cells — cells that release somatostatin, an inhibitor of gastrin.
  • ECL Cells — enterochromaffin-like cells that secrete histamine.
  • Vagus Nerve — cranial nerve that stimulates gastric secretion via acetylcholine and GRP.
  • Alkaline Tide — increase in blood pH due to bicarbonate release post-acid secretion.
  • Mucosal Barrier — protective lining in the stomach preventing self-digestion.

Action Items / Next Steps

  • Review mechanisms of the intestinal phase for the next lecture.
  • Study diagrams of stomach cell types and signaling pathways for clarity.