Gastric inhibitory polypeptide stimulated secretion of somatostatinlike immunoreactivity from the stomach: inhibition by acetylcholine or vagal stimulation

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Abstract
The possible involvement of gastric somatostatin-like immunoreactivity (SLI) in the acid inhibitory action of gastric inhibitory polypeptide (GIP) was studied in an isolated perfused rat stomach. GIP, in a dose of 5 or 50 ng/ml, caused a 4- and 12-fold increase in SLI secretion, respectively. At the higher dose level the stimulated secretory rate declined throughout the perfusion suggesting that secretion exceeded the capacity to synthesize SLI under excessive GIP stimulation. Acetylcholine (10 .mu.M) or vagal stimulation (7 V, 10 Hz, 5 ms) completely inhibited GIP-stimulated SLI secretion. The acid inhibitory activity of GIP is probably mediated via release of gastric SLI and this action is under cholinergic control.