AJP - Gastrointestinal and Liver Physiology, Vol 247, Issue 3 248-G252, Copyright © 1984 by American Physiological Society
Gastrin release from isolated perfused rat stomach after vagotomy
R. A. Pederson, Y. N. Kwok, A. M. Buchan, C. H. McIntosh and J. C. Brown
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.
