Gastric Secretion And Digestion In The Stomach Notes

Lecture 7 & 8

Gastric secretion and digestion in the stomach

• Basic functions of stomach digestion

  • Reservoir- Gastric motility

  • Digest proteins- Pepsins

  • Essential for vit B12 absorption- Intrinsic factor (cells of the corpus)

• Gastric secretion

  • 1.5-2.5 litres per day; pH 0.9-1.5

  • Composition: HCl, pepsins (pepsinogen first), intrinsic factor, mucus & HCO3- (keeps lining of stomach intact in presence of acid)

• Gastric mucosa divided into 3 regions

  • CARDIAC GLANDULAR REGION

    • Main function is mucus secretion

    • Not very many acid secreting cells

  • OXYNIC GLANDULAR REGION

    • Few gastrin & histamine producing cells (regulatory molecules)

    • Secrete: HCl, intrinsic factor, pepsinogens, mucus, histamine

  • PYLORIC GLANDULAR REGION

    • Secrete: Mucus, Gastrin, Somatostatin (last two= regulatory molecules)

    • Won’t see gland producing acid

• Structure of gastric mucosa

  • Gastric pits (G cells)= Gastrin

  • Surface epithelial cells= Mucus, HCO3-

  • Mucus neck cells= Mucus

  • Parietal cell= HCl, Intrinsic factor

  • Chief cell= Pepsinogens

  • Endocrine cells= Histamine (ECL cell), Somatostatin (D cell)

• Secretion of HCl

  • Function of HCl

    • Promote pepsin activation (from pepsinogen)

    • Kill/inhibit microorganisms

    • Stimulate secretions in small intestine

    • Helps iron & calcium absorption in small intestine (WON’T BE TESTED)

  • Morphological changes that accompany HCl secretion

    • Resting parietal cells

      • Tubulovesicles (released into apical membrane, signal)

      • Not a large surface area (no finger like projections)

    • Active parietal cells

      • Larger secretory membrane, more H+ pumps, K+ and Cl- channels

      • Increase in surface area (finger like projections)

      • Total transport across membrane= Number transporters X Active

  • Cellular mechanisms of HCl secretion

    1. H+/K+ ATPase uses energy to pump out H+ ions into lumen and K+ in

    2. Apical membrane K+ channels recycle K+ ions across apical membrane

    3. H+ secretion causes intracellular pH to rise. Rise in pH= passive uptake of CO2 and H2O across basolateral membrane. Combine to produce HCO3- and H+, catalysed by carbonic anhydrase

    4. HCO3- ions removed across basolateral membrane by Cl-/HCO3- exchanger

    5. HCO3- exit causes alkalinisation of BVs (ALKALINE TIDE)

    6. Cl- ions that enter exit passively across apical membrane completing HCL secretion

    7. Na+/K+ ATPase creates inward directed Na+ gradient across basolateral membrane (used for other pathways)

    8. Basolateral K+ channels maintain force for Cl- to exit (apical membrane)

  • Regulation of HCl secretion

    • Direct regulation

      • ACh

        • Uses Ca2+ for signalling

        • PSNS= Vagovagal reflex

        • Indirectly effects G cells and ECL cells

      • Histamine

        • Released from ECL cells

        • Gastric glands close to parietal cells

        • Uses cAMP for signalling

      • Gastrin

        • G cells in pyloric area

        • Into BVs

        • Uses Ca2+ for signalling

      • Somatostatin

        • TURNS OFF THE PROCESS

        • D cells

        • Inhibits Ca2+

• Secretion of…

  • Intrinsic factor

    • ONLY GASTRIC SECRETION ESSENTIAL FOR LIFE

    • Vit. B12 protected by intrinsic factor (stop digestion by pancreatic proteases)

    • Glycoprotein secreted by parietal cells of stomach

    • Facilitates absorption of B12 in ileum

  • Pepsins

    • Digest proteins (to peptides)

    • Optimal pH <3 (process working well and activation of pepsinogen)

    • Pepsinogen secreted by chief cells (HCl turns it to pepsin & helps activity)

  • Mucus & bicarbonate

    • Mucus secreted from mucus neck cell and surface epithelial cell

      • From tightly packed configuration to long stringy formation (helped by HCO3-)

    • HCO3- secreted from surface epithelial cells

      • Taken into cells across basolateral using Na+ co-transporter

      • Exit across apical membrane using Cl- co-transporter

    • Both stimulated by enteric NS (PSNS- ACh), so Ca2+ stimulated release

• Why don’t HCl and pepsins damage gastric mucosa?

  • Physiological barrier- Gastric mucosal barrier

    • Diffusion barrier ~200µm thick

    • Mucous gel & HCO3-

    • Low HCO3- conc. at top, high at the bottom (near epithelial cells)

  • Anatomical barrier- Epithelial cells

    • Tight junctions impermeable to acid

• What happens when gastric mucosal barrier is damaged? GASTRIC ULCERS

  • H+ and pepsin attack...

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