Stomach acid (gastric acid) secretion is primarily controlled by three local hormones: acetylcholine, gastrin, and histamine.
Here's a more detailed breakdown:
1. The Three Key Players:
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Acetylcholine: This neurotransmitter has the largest effect on gastric acid production. It's released in response to vagus nerve stimulation, which occurs when you think about, smell, or taste food. Acetylcholine stimulates parietal cells (which produce acid), G cells (which produce gastrin), and enterochromaffin-like (ECL) cells (which release histamine).
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Gastrin: This hormone is secreted by G cells in the stomach antrum. Gastrin stimulates parietal cells directly to produce acid and also stimulates ECL cells to release histamine. Gastrin release is stimulated by the vagus nerve, peptides and amino acids in the stomach.
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Histamine: This hormone is released by ECL cells. Histamine strongly stimulates parietal cells to produce acid.
2. How These Hormones Interact:
The stimulation of stomach acid secretion is a complex process involving the interplay of these three hormones. Here's a simplified sequence of events:
- Vagal Stimulation: When you anticipate or consume food, the vagus nerve is stimulated.
- Acetylcholine Release: The vagus nerve releases acetylcholine.
- Multiple Cell Stimulation: Acetylcholine stimulates parietal cells, G cells, and ECL cells.
- Gastrin Release: G cells release gastrin.
- Histamine Release: ECL cells release histamine.
- Acid Production: Parietal cells are stimulated by acetylcholine, gastrin, and, most significantly, histamine, leading to the production and secretion of hydrochloric acid (HCl), which is the main component of stomach acid.
3. Inhibition of Acid Secretion:
The body also has mechanisms to inhibit gastric acid secretion when it's no longer needed. This involves hormones such as somatostatin, which inhibits the release of gastrin and histamine, and prostaglandin, which directly inhibits parietal cell acid production.
4. Summary Table:
| Hormone | Source | Action |
|---|---|---|
| Acetylcholine | Vagus nerve | Stimulates parietal cells, G cells, and ECL cells; major driver of acid secretion. |
| Gastrin | G cells | Stimulates parietal cells and ECL cells. |
| Histamine | ECL cells | Potently stimulates parietal cells to produce acid. |
| Somatostatin | D cells in the stomach and duodenum | Inhibits gastrin and histamine release; reduces acid secretion. |
| Prostaglandins | Stomach Lining | Directly inhibits parietal cell acid production, also protects the lining of the stomach. |
5. Clinical Relevance:
Understanding the control of stomach acid is crucial for managing conditions like:
- Peptic Ulcers: Excessive acid can erode the stomach or duodenal lining.
- Gastroesophageal Reflux Disease (GERD): Acid refluxes into the esophagus, causing heartburn.
- Zollinger-Ellison Syndrome: A rare condition where tumors produce excessive gastrin, leading to very high acid levels.
Medications like proton pump inhibitors (PPIs) directly block acid production by parietal cells, while H2 receptor antagonists block the action of histamine on parietal cells. These drugs are commonly used to treat conditions related to excessive stomach acid.
