Effect of vagus, gastric inhibitory polypeptide, and HCl on gastrin and somatostatin release from perfused pig antrum.
The porcine antrum was isolated with the pancreas and perfused in vitro with an artificial medium supplemented with erythrocytes. The vagal innervation was preserved. Effluent was collected from the portal vein as well as from a vein directly draining the antrum. Electrical vagal stimulation increased gastrin output and inhibited somatostatin output. Intraluminal hydrochloric acid had the opposite effect. Gastric inhibitory polypeptide (GIP) in physiological concentrations (90 and 450 pmol/l) increased somatostatin output, inhibited gastrin output, and potentiated the effect of HCl on somatostatin release. Vagal stimulation, however, abolished the GIP effect on somatostatin output. Thus gastrin and somatostatin outputs were always inversely affected by the applied stimuli, suggestive of somatostatin-mediated control of gastrin secretion. GIP may exert its effects via local somatostatin release.
D000818:Animals; D004558:Electric Stimulation; D005749:Gastric Inhibitory Polypeptide / Q000494:pharmacology*; D005753:Gastric Mucosa / Q000187:drug effects / Q000378:metabolism; D005755:Gastrins / Q000378:metabolism*; D005768:Gastrointestinal Hormones / Q000494:pharmacology*; D006851:Hydrochloric Acid / Q000494:pharmacology*; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000187:drug effects / Q000378:metabolism; D007700:Kinetics; D011706:Pyloric Antrum / Q000187:drug effects / Q000378:metabolism*; D013004:Somatostatin / Q000378:metabolism*; D013552:Swine; D014630:Vagus Nerve / Q000502:physiology*
D005755:Gastrins; D005768:Gastrointestinal Hormones; D007328:Insulin; D013004:Somatostatin; D005749:Gastric Inhibitory Polypeptide; D006851:Hydrochloric Acid