Related Experiment Videos
Physiological significance of ECL-cell histamine
K Andersson1, D Chen, H Mattsson
1Astra Hässle AB, Mölndal, Sweden. kjell.andersson@hassle.se.astra.com
The Yale Journal of Biology and Medicine
|August 26, 1999
Summary
Gastrin stimulates gastric acid secretion via ECL cell histamine, but vagal stimulation does not. Gastrin
Area of Science:
- Gastroenterology
- Physiology
- Pharmacology
Background:
- Histamine in the stomach's oxyntic mucosa is stored in enterochromaffin-like (ECL) cells and mast cells.
- ECL cells contain the majority (at least 80%) of histamine in rat oxyntic mucosa.
- Histamine plays a crucial role in regulating gastric acid secretion.
Purpose of the Study:
- To investigate the role of ECL cell histamine in mediating gastric acid secretion.
- To determine if ECL cell histamine is essential for gastrin- and vagally-induced acid secretion.
- To examine whether gastrin's trophic effects on the oxyntic mucosa depend on ECL cell histamine.
Main Methods:
- Depletion of ECL cell histamine using alpha-fluoromethylhistidine (alpha-FMH).
- Measurement of basal, gastrin-stimulated, and vagally-induced gastric acid secretion.
- Induction of long-term hypergastrinemia combined with alpha-FMH infusion.
Main Results:
- Depletion of ECL cell histamine reduced basal acid secretion and abolished gastrin-stimulated secretion.
- Vagally-induced acid secretion was unaffected by alpha-FMH but inhibited by an H2 antagonist.
- Gastrin-evoked trophic effects on the oxyntic mucosa were independent of ECL cell histamine.
Conclusions:
- Gastrin stimulates gastric acid secretion primarily through the release of histamine from ECL cells.
- Vagally-induced acid secretion, while histamine-dependent, does not rely on ECL cell histamine.
- Gastrin's trophic effects on the stomach are independent of ECL cell histamine.