Electron microscopy provided a conclusive diagnosis of ECL cell tumours in two cases.

ECL cells synthesize and secrete histamine.

The most important inhibitor of the ECL cell is somatostatin from oxyntic D cells.

It activates parietal cells to release acid and ECL cells to release histamine.

Gastrin is transferred from a specific type of G cell in the gastric epithelium to the ECL cells by blood.

Although ECL cell type was predominant in all tumours, other endocrine cell types have been noted in two tumours.

Cephalic phase cause ECL cells to secrete histamine and increase HCl acid in the stomach.

ECL cells respond to gastrin released by G-cells and they release histamine, which will stimulate the parietal cells to produce gastric acid.

However, ECL cells are activated directly by ACh on M1 receptors from direct vagal innervation leading to histamine release.

Gastrin is more important indirectly by increasing histamine synthesis in ECL cells, as gastrin has no effect on the maximum histamine-stimulated gastric acid secretion.

On oxyntic tissue sections, argyrophil endocrine cells (mainly ECL cells) were stinaed with the Grimelius silver impregnation technique.

Tumoral ECL cells were either typical, containing vesicular electron dense granules or atypical with non-vesicular granules displaying a coarsely granular structure.

The clinical and biological profiles of Zollinger-Ellison sydrome patients who develop fundic ECL cell tumours cannot be determined from the study of such a small number of cases.

In the lamina propria of the body of the stomach the ACh released from the vagal endings triggers histamine secretion from ECL cells.

Gastrin stimulates acid secretion by directly stimulating parietal cells as well as by promoting histamine secretion by ECL cells.

G cells are stimulated by vagal stimulation through the neurotransmitter gastrin-releasing peptide; this causes the G cells to secrete gastrin, which in turn stimulates ECL cells to release histamine.

Enterochromaffin-like cells or ECL cells are a type of neuroendocrine cells found in the gastric glands of the gastric mucosa beneath the epithelium, in particular in the vicinity of parietal cells.

One, the parietal cells in the body of the stomach are stimulated to release H. Two, the ECL cells of the lamina propria of the body of the stomach are stimulated to release histamine.

Indeed, lifelong hypergastrinaemia, induced by long term administration of inhibitors of gastric acid secretion or partial fundectomy as well as exogenous gastrin administration, have been associated with pronounced hyperplasia of gastric argyrophil cells or development of ECL cell carcinoids in rats.

Gastrin exerts a trophic effect on enterochromaffin-like cells (ECL cells are responsible for histamine secretion) and is hypothesized to be one mechanism to explain the malignant transformation of ECL cells into carcinoid tumors in AMAG.

This is done both directly on the parietal cell and indirectly via binding onto CCK2/gastrin receptors on ECL cells in the stomach, which then responds by releasing histamine, which in turn acts in a paracrine manner on parietal cells stimulating them to secrete H+ ions.

A mixed population of ECL cells and cells resembling P cells by the granule size was observed in patient no 5 while very heterogeneous cellular proliferation with a prominent ECL cell component was found in a fourth case (case no 1).