Gastric Acid Secretion – Regulation & Output
GASTRIC ACID SECRETION – REGULATION & OUTPUT
- Gastric acid – Secreted by gastric glands in gastric mucosa.
GASTRIC GLANDS IN STOMACH:
1. In pyloric & cardiac regions:
- Gastric glands are “Mucous” type.
- Secrete only mucous & HCO3–.
- In pylorus referred “Mucus-secreting pylorus gland”.
- Contains less parietal & chief cells.
2. In body & fundus regions:
- Glands contain secretory cells.
Cell types:
2a. Parietal/Oxyntic cells –
- Secrete hydrochloric acid (HCl) & Intrinsic factor of castle.
2b. Chief/Zymogen/Peptic cells –
- Secrete pepsinogen.
2c. G cells –
- Secretes Gastrin.
2d. Delta (D) cells –
- Secretes Somatostatin.
2e. Entero-chromaffin like (ECL) cells –
- Secretes Histamine.
COMPOSITION OF GASTRIC ACID:
- In human – 2.5 L (105ml/hr) gastric juice secreted daily.
- Gastric acid pH is less than 3 (usually 1-2).
Important constituents:
- HCl (H+ & Cl–).
- Anions (HPO4-2 & SO4+2).
- Cations (Na2+, K+, & Mg2+).
- Pepsinogen & Pepsin.
- Mucus.
- Lipase.
- Intrinsic factor of castle.
REGULATION OF ACID SECRETION:
- Gastric acid secreted by parietal cell activation in gastric mucosa.
1. ACTIVATORS FOR ACID SECRETION:
- Mainly Histamine – H2 receptors.
- Acetylcholine (M3 receptor).
- Gastrin.
Mechanism:
Ach & gastrin acts indirectly.
- By releasing histamine.
- Also by stimulating H+-K+-ATPase (proton pump).
Vagal (Parasympathetic) stimulation –
- Increases acid secretion.
- Through acetylcholine.
Clinical application:
Proton Pump/H+ inhibitors:
- By blocking H+ receptors/inhibiting proton pump –> Blocking acid secretion.
Anti-muscarinic drugs:
- Blocks muscarinic receptors.
- Ex: Pirenzepine.
2. INHIBITORS OF ACID SECRETION:
- Somatostatin –.
- By directly inhibiting parietal cells & gastrin secretion
- Secretin
- Cholecystokinin (CCK).
- GIP & VIP –
- Inhibit gastric secretion by stimulating somatostatin release.
PGE2 –
- By inhibiting parietal cells & gastrin release.
- Best established inhibitor – Low pH (Acid itself).
- Stomach & duodenal acidification inhibits acid secretion.
- By inhibiting gastrin release from G cells.
CONDITIONS:
1. Increased gastric acid secretion:
- In duodenal ulcer.
- Gastric ulcer.
- ZES.
2. Reduced gastric acid secretion:
- After vagotomy.
- In Pernicious anemia.
GASTRIC ACID OUTPUT:
- Measurement of gastric acid output – Clinical importance.
- Two important parameters –
1. Basal Acid Output (BAO) –
- Rate of acid secretion in absence of any stimulations.
- Normal BAO – < 10 (2 – 5) mmol/hr.
2. Maximal Acid Output (MAO)/Total Acid Output –
- Rate of acid secretion produced by stimulants like histamine/ pentagastrin.
- Normal MAO – < 50 mmol/hr.
- Values reflects total parietal cell population in stomach.
- Hence, referred “Parietal cell mass”.
GASTRIC ACID SECRETION – REGULATION & OUTPUT
- Parietal/Oxyntic cells secrete Hydrochloric acid (HCl) & Intrinsic factor of castle.
- Chief/Zymogen/Peptic cells secretes pepsinogen.
- Delta (D) cells secrete Somatostatin.
- Pylorus contains “mucus-secreting pylorus gland”.
- In human – 2.5 L (105ml/hr) gastric juice secreted daily.
- Important cationic constituents in acid – Na2+, K+, & Mg2+.
- Main activators of acid secretion are mainly Histamine (H2 receptors), Acetylcholine (M3 receptor) & Gastrin.
- Vagal (Parasympathetic) stimulation increases acid secretion through acetylcholine.
- Proton Pump/H+ inhibitors act by blocking H+ receptors.
- Inhibitors of acid secretion are Somatostatin, Secretin, Cholecystokinin (CCK), GIP & VIP.
- Best established inhibitor of acid secretion is “Low pH” (Acid itself).
- Normal BAO – < 10 (2 – 5) mmol/hr.
- Maximal Acid Output (MAO)/Total Acid Output values reflect total parietal cell population in the stomach, hence referred “Parietal cell mass”


