In the oxyntic mucosa of the mammalian stomach, histamine is stored in ECL
cells and in mucosal mast cells. In the rat, at least 80 percent of oxyntic
mucosal histamine resides in the ECL cells. Histamine is a key factor in t
he regulation of gastric acid secretion. Following depletion of ECL-cell hi
stamine by treatment with alpha-fluoromethylhistidine (alpha-FMH), basal ac
id secretion was reduced, and gastrin-stimulated acid secretion was abolish
ed. Vagally-induced acid secretion (by insulin injection or pylorus ligatio
n) was unaffected by alpha-FMH treatment but inhibited by an H-2 antagonist
. These results suggest that gastrin stimulates acid secretion via release
of ECL-cell histamine, whereas vagally-induced acid secretion-although hist
amine-dependent-does not rely on ECL-cell histamine. Gastrin is known to ha
ve a trophic effect on the oxyntic mucosa. By combining long-term hypergast
rinemia with continuous infusion of alpha-FMH, we were able to show that ga
strin-evoked trophic effects in the stomach do not depend on ECL-cell hista
mine.