Gastric Acid Secretion Physiology Animation: Video

Gastric glands

3 types:
  1. Cardiac: small in number and secretes mucin
  2. Fundic and Body: highest in number and secretes acid juice secretion
  3. Pyloric: mucous type
A typical acid secreting gland is tubular and straight.
Each gland is divided into 3 parts: Neck, Body and Base.
Mucous membrane is maintained by dynamic equilibrium between production and desquamation of its cells.

Gastric gland cells and their secretion:
  1. Chief cells of Peptic cells: Pepsinogens
  2. Oxyntic or parietal cells: HCl and intrinsic factor
  3. Amine precursor uptake and decarboxylation (APUD) cells: Gastrointestinal hormones
  4. Mast cells: Histamine
  5. Argentaffin cells: serotonin
  6. 'G' cells: Gastrin
  7. 'D' cells: Somatostatin
  8. Neck and isthmus cells: Mucin
Phases of Gastric secretion:

Cephalic phase (20%)
  • occurs even before food enters the stomach
  • stimuli for unconidtioned reflex: presence of food in mouth, taste of food, act of chewing, act of swallowing
  • stimuli for conditioned reflex: sight, thought, smell of food
  • signals originate in cerebral cortex and in appetite centers of amygdala and hypothalamus
  • signal ---> dorsal motor nuclei of vagi ---> vagus nerve ---> stomach
  • starts with a latency of < 5 min and continues for 30 to 120 min
  • rate of secretion: 250 to 750 ml/hour
  • secretion of psychic or appetite juice: rich in acid and pepsin with high digestive power
Gastric phase (70%)
  • once food enters the stomach, it excites:
  1. Long vagovagal reflex: from stomach to the brain and back to the stomach (afferent and efferent both being vagal fibers)
  2. Short local enteric reflexes
  3. Gastrin mechansim
  • starts with a latency of 15 minutes and continues as long as there is food in the stomach
  • composition of juice depends upon the composition of food
  • rate of secretion: 40 to 70 ml/hour
Intestinal phase (10%)
  • begins with the presence of food in the upper portion of small intestine 
  • chemicals involved: bombesin and gastrin
  • starts with a latency of 2 to 3 hours and continues for 8 to 10 hours
  • rate of secretion: 40 to 60 ml/hour
  • inhibitory influences operate:
i) Neural inhibition-
  1. increased fat content, tonicity, volume of chyme in small intestine
  2. enterogastric reflex
ii) Chemical inhibition-
  1. chalone: secretin, neurotensin, CCK-Pz, prostaglandins, VIP, GIP, etc.
  2. enterogastrone
Interdigestive phase
  • when there is no food either in stomach or small intestine
  • basal secretion: resting acid secretion
  • mainly mucus, little pepsin and lamost no acid
  • emotional stimuli increase this secretion (highlt peptic and acidic) leading to peptic ulcers
  • mechanism similar to cephalic phase

Parietal or Oxyntic Cells:
  • situated mainly towards neck of glands
  • secrete hydrochloric acid (HCl) and intrinsic factor
  • cells have an extensive microcanlicular system which communicates with the lumen of the gland by a canaliculus
  • in resting stage of cell, part of the microcanalicular system is converted into the tubulovesicular structures (vesicles are fused with the microcanalicular system when cell is stimulated to secrete HCl)
HCl secretion:

The H+/K+-ATPase in the luminal membrane of parietal cells drives H+ ions into the glandular lumen in exchange for K+ (primary active transport), thereby raising the H+ conc. in the lumen. K+ taken up in the process circulates back to the lumen via luminal K+ channels. For every H+ ion secreted, one HCO3– ion leaves the blood side of the cell and is exchanged for a Cl– ion via an anion antiporter. (The HCO3 – ions are obtained from CO2+ OH–, a reaction catalyzed by carbonic anhydrase, CA). This results in the intracellular accumulation of Cl– ions, which diffuse out of the cell to the lumen via Cl– channels. Thus, one Cl– ion reaches the lumen for each H+ ion secreted.

Regulation of gastric acid secretion:

Factors that stimulate gastric acid secretion
  1. ACh directly activates parietal cells in the fundus (M3 cholinoceptors).
  2. GRP (gastrin-releasing peptide) released by neurons stimulates gastrin secretion from G cells in the antrum. Gastrin released in to the systemic circulation in turn activates the parietal cells via CCKB receptors (= gastrin receptors).
  3. The glands in the fundus contain H (histamine) cells or ECL cells (enterochromaffin– like cells), which are activated by gastrin (CCKB receptors) as well as by ACh and adrenergic substances. The cells release histamine, which has a paracrine effect on neighboring parietal cells (H2 receptor). Local gastric and intestinal factors also influence gastric acid secretion because chyme in the antrum and duodenum stimulates the secretion of gastrin.

Factors that inhibit gastric acid secretion:

  1. Low pH
  2. Distension of duodenum
  3. Fat and protein breakdown products in duodenum
  4. Somatostatin
  5. Secretin
  6. Prostaglandin
  7. Gastric Inhibitory Peptide (GIP)
  8. Vasoactive Intestinal Peptide (VIP)

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