Postvagotomy hypergastrinemia persists in the isolated perfused rat stomach, but its cause is unknown. The possible role of cholinergic nervous pathways was investigated in the isolated vascularly perfused rat stomach after vagotomy. Atropine and hexamethonium, but not propranolol, inhibited postvagotomy hypergastrinemia. A nervous mechanism involving acetylcholine was further suggested by the inhibitory action of methionine-enkephalin on gastrin release after vagal section. Methacholine, a muscarinic receptor agonist, only weakly stimulated gastrin release from vagotomized stomachs when compared with shamoperated controls, indicating that a cholinergic drive was already in place. Immunocytochemical studies of antral tissue following vagotomy indicated that numbers of gastrin-containing cells (G-cells) were not increased after vagotomy but exhibited reduced intensity of gastrin staining when compared with control stomachs. It was concluded that basal hypergastrinemia may result from increased stimulation of a normal G-cell population by a cholinergic mechanism at the ganglionic level.
- Copyright © 1984 the American Physiological Society