Control factors in the release of gastrin by direct electrical stimulation of the vagus.
The release of gastrin by direct electrical stimulation of the vagus was studied together with the relative effects on the response of antral and duodenal acidification. As expected, gastrin levels increased to three times the normal simulated response following antral neutralization. In contrast, duodenal acidification failed to influence the vagal release of gastrin when the antrum was neutralized although it had a minor effect when the antrum was acidified. Thus the antral pH dominates over duodenal pH as a factor in controlling gastrin release. Surprisingly, atropine in doses which blocked acid release and produced marked cardiac effects failed to inhibit the release of gastrin from the antrum on vagal stimulation. This suggests that, using this model, vagal release of gastrin, if cholinergic, is highly resistant to atropine.
D000818:Animals; D001285:Atropine / Q000494:pharmacology; D004285:Dogs; D004386:Duodenum; D004558:Electric Stimulation; D005260:Female; D005750:Gastric Juice / Q000378:metabolism; D005755:Gastrins / Q000378:metabolism*; D006339:Heart Rate; D006801:Humans; D006863:Hydrogen-Ion Concentration; D011706:Pyloric Antrum; D011817:Rabbits / Q000276:immunology; D011863:Radioimmunoassay; D012636:Secretory Rate / Q000187:drug effects; D013156:Splenectomy; D014630:Vagus Nerve / Q000502:physiology*
D005755:Gastrins; D001285:Atropine