Gastric inhibitory polypeptide stimulated secretion of somatostatinlike immunoreactivity from the stomach: inhibition by acetylcholine or vagal stimulation.
The possible involvement of gastric somatostatinlike 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 microM) or vagal stimulation (7 V, 10 Hz, 5 ms) completely inhibited GIP-stimulated SLI secretion. It is therefore proposed that the acid inhibitory activity of GIP is probably mediated via release of gastric SLI and this action is under cholinergic control.
D000109:Acetylcholine / Q000494:pharmacology*; D000818:Animals; D004558:Electric Stimulation; D005749:Gastric Inhibitory Polypeptide / Q000494:pharmacology*; D005753:Gastric Mucosa / Q000294:innervation / Q000378:metabolism*; D005768:Gastrointestinal Hormones / Q000494:pharmacology*; D008297:Male; D051381:Rats; D013004:Somatostatin / Q000276:immunology / Q000378:metabolism*; D013997:Time Factors; D014630:Vagus Nerve / Q000502:physiology*
D005768:Gastrointestinal Hormones; D013004:Somatostatin; D005749:Gastric Inhibitory Polypeptide; D000109:Acetylcholine