Function


ECL cells synthesize in addition to secrete histamine. These cells are stimulated by the hormones gastrin not depicted in the adjacent diagram & pituitary adenylyl cyclase-activating peptide. G cells are stimulated by vagal stimulation through the neurotransmitter gastrin-releasing peptide; this causes the G cells to secrete gastrin, which in remake stimulates ECL cells to release histamine. Note that this circuit is non activated by acetylcholine, which is of particular importance because the supervision of atropine will not block the vagal stimulation of the G cells, as ACh is not the neurotransmitter for these cells.

However, ECL cells are activated directly by ACh on M1 receptors from direct vagal innervation leading to histamine release. This pathway will be inhibited by atropine.

Gastrin is transferred from a specific type of G cell in the gastric epithelium to the ECL cells by blood. Histamine and gastrin act synergistically as the almost important stimulators of hydrochloric acid secretion from parietal cells and stimulators of secretion of pepsinogen from chief cells. The almost important inhibitor of the ECL cell is somatostatin from oxyntic D cells.

Enterochromaffin-like cells also form pancreastatin and probably other peptide hormones and growth factors.