Effects of various gastrointestinal peptides on parietal cells and endocrine cells in the oxyntic mucosa of rat stomach.

Abstract

SUMMARY1. The effects of secretin, glucagon, cholecystokinin-pancreozymin (CCK-PZ), gastric inhibitory peptide (GIP), vasoactive intestinal peptide (VIP), somatostatin, neurotensin and enkephalin on basal, pentagastrin-and histamine-stimulated gastric acid secretion were investigated in the conscious fistula rat.2. Glucagon and GIP were ineffective inhibitors of basal and pentagastrinstimulated secretion. CCK-PZ stimulated acid scretion at a low dose level but at higher doses it inhibited both pentagastrin-and histamine-induced secretions. VIP was ineffective at low doses and at high doses its action was complicated by reflux of stimulated pancreatic and intestinal secretions into the stomach. Met-enkephalin inhibited histamine-but not pentagastrin-stimulated secretion. Neurotensin inhibited the response to pentagastrin but had no effect on histamine-stimulated secretion. Secretin and somatostatin were potent inhibitors of basal and pentagastrinstimulated acid secretion with little or no effect on the response to histamine.3. At doses completely inhibitory to pentagastrin-stimulated secretion secretin and somatostatin did not block the mobilization of gastric mucosal histamine by pentagastrin, although somatostatin caused partial competitive inhibition at lower doses of pentagastrin. Thus secretin and somatostatin inhibited pentagastrin-induced secretion neither by blocking gastric mucosal histamine mobilization nor by abolishing the direct action of histamine on the parietal cell -findings which are inconsistent with the proposed role of histamine as the mediator of the action of gastrin on the parietal cell.

Influence of exogenous glucagon on gastric acid secretion, mucosal blood flow, and stress ulcers in the rat: Dose-response results under non-stress conditions and immobilization stress

“…The lack of acid inhibition is in accordance with other reports for the latter species [6,13]. In view of the levels of plasma glucagon achieved by exogenous infusion this means that glucagon (1) cannot be generally accepted as an enterogastrone and (2) might play a biologic role in pepsin secretion by chief cells.…”

Effect of somatostatin, secretin, and glucagon on secretagogue stimulated aminopyrine uptake in isolated canine parietal cells

“…Somatostatin has been shown to inhibit gastrin release from the G cells and to partially block the pentagastrin depletion of histamine in the rat stomach [13]. The above findings suggest that somatostatin can modulate gastric acid secretion by interfering with the release of secretagogues.…”