Pancreatic polypeptide stimulates gastric acid secretion through a vagal mechanism in rats.
The present study examined the effect of pancreatic polypeptide (PP) on gastric acid secretion. A 45-min infusion of PP was delivered into the jugular vein of urethan-anesthetized rats. Rat PP (100 pmol) significantly increased acid secretion over baseline; bilateral cervical vagotomy or peripheral atropine both eliminated this acid response. Neither intraperitoneal infusion nor close intra-arterial infusion of 100 pmol PP into the gastric circulation altered acid secretion. These results suggest that although PP requires intact vagal reflexes to stimulate acid output, it does not act on afferent or presynaptic efferent terminals of the vagus or directly within the stomach. Given that vagal reflexes consist of an afferent limb, an efferent limb, and a central relay, it may be that the target of circulating PP lies within the central nervous system. Indeed, previous studies from our laboratory have shown that microinjection of PP into the dorsal vagal complex results in long-lasting vagal-dependent elevation of gastric acid secretion.
McTigue
D M
DM
Department of Physiology, Ohio State University, Columbus 43210, USA.
Rogers
R C
RC
D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001933:Brain Stem / Q000502:physiology*; D002417:Cattle; D005744:Gastric Acid / Q000378:metabolism*; D007262:Infusions, Intravenous; D007269:Injections, Intra-Arterial; D007274:Injections, Intraperitoneal; D008297:Male; D010191:Pancreatic Polypeptide / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D014628:Vagotomy; D014630:Vagus Nerve / Q000502:physiology*
D010191:Pancreatic Polypeptide; D001285:Atropine