Spinal and peripheral modulation of gastric acid secretion and arterial pressure by neuropeptide Y, peptide YY, and pancreatic polypeptide in rats

Peptides ◽  
1993 ◽  
Vol 14 (6) ◽  
pp. 1299-1308 ◽  
Author(s):  
S.A. Wager-Pagé ◽  
G. Rosenbaum ◽  
W.L. Veale ◽  
J.S. Davison
Keyword(s):  
Arterial Pressure ◽  
Acid Secretion ◽  
Neuropeptide Y ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Pancreatic Polypeptide ◽  
Peptide Yy

Peptide YY interacts with secretin and duodenal acidification to inhibit gastric acid secretion

1987 ◽  
Vol 18 (3-4) ◽  
pp. 155-163 ◽  
Author(s):  
Felix Lluis ◽  
Guillermo Gomez ◽  
Masaki Fujimura ◽  
George H. Greeley ◽  
Courtney M. Townsend ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Peptide Yy ◽  
Duodenal Acidification

Effects of Acute Cold Pressor Test on Vagally Stimulated Gastric Acid Secretion and Circulating Levels of Human Pancreatic Polypeptide and Gastrin

Digestion ◽  
1994 ◽  
Vol 55 (3) ◽  
pp. 154-159 ◽  
Author(s):  
Anna Paternicò ◽  
Vincenzo Stanghellini ◽  
Roberto De Giorgio ◽  
Pasquale Santaguida ◽  
Maurizio Capelli ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Pancreatic Polypeptide ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Pressor Test ◽  
Human Pancreatic Polypeptide ◽  
Circulating Levels

Structural requirements of peptide YY for biological activity at enteric sites

1992 ◽  
Vol 263 (5) ◽  
pp. G695-G701 ◽  
Author(s):  
K. Yoshinaga ◽  
T. Mochizuki ◽  
N. Yanaihara ◽  
K. Oshima ◽  
M. Izukura ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Insulin Release ◽  
Peptide Yy ◽  
Exocrine Secretion ◽  
Pancreatic Exocrine Secretion ◽  
Structural Requirements ◽  
Pancreatic Exocrine

Peptide YY (PYY) is a colonic hormone consisting of 36 amino acids that is a potent inhibitor of pancreatic exocrine, gastric acid, and insulin secretion. The objective of the present experiments was to characterize the structural requirements of PYY for inhibition of pancreatic exocrine, gastric acid, and insulin secretion, using conscious dogs prepared with gastric and pancreatic fistulas. Intravenous administration of PYY-(1-36), PYY-(3-36), or PYY-(4-36) (400 pmol.kg-1 x h-1) inhibited cholecystokinin-8-stimulated (25 pmol.kg-1 x h-1) pancreatic exocrine secretion (P < 0.05); however, PYY-(1-10), PYY-(1-20), PYY-(6-36), PYY-(10-36), PYY-(13-36), PYY-(24-36), and PYY-(27-36) did not inhibit pancreatic exocrine secretion. Intravenous administration of PYY-(1-36), PYY-(3-36), or PYY-(4-36) (200, 400, 800 pmol.kg-1 x h-1) inhibited pentagastrin (0.5 microgram.kg-1 x h-1)-stimulated gastric acid secretion (P < 0.05), as well as 2-deoxy-D-glucose-stimulated insulin release (75 mg/kg) in a dose-related manner. PYY-(6-36), PYY-(13-36), and [Leu31, Pro34] neuropeptide Y did not inhibit either gastric acid secretion or insulin release. In the gastric acid and insulin secretion bioassays, PYY-(1-36) was significantly more potent than PYY-(3-36) and PYY-(4-36); however, in the pancreatic exocrine secretion bioassay, the inhibitory effects of PYY-(3-36) and PYY-(1-36) did not differ significantly. PYY-(4-36) was less potent than PYY-(1-36) on pancreatic exocrine secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

PYY in brain stem nuclei induces vagal stimulation of gastric acid secretion in rats

1995 ◽  
Vol 268 (6) ◽  
pp. G943-G948 ◽  
Author(s):  
H. Yang ◽  
Y. Tache
Keyword(s):  
Acid Secretion ◽  
Brain Stem ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Serotonin Receptor ◽  
Peptide Yy ◽  
Motor Nucleus ◽  
Dorsal Motor Nucleus ◽  
Raphe Pallidus ◽  
Stimulation Of

The influence of peptide YY (PYY) microinjected into brain stem nuclei on gastric acid secretion (GAS) was investigated in urethan-anesthetized rats with gastric cannula. PYY (30-200 ng) microinjected into the dorsal motor nucleus of the vagus (DMN) induces a dose-related and vagal-dependent stimulation of GAS (net increase from 13 +/- 4 to 59 +/- 12 mumol/90 min). PYY (200 ng) injected intravenously intracisternally into sites adjacent to the DMN had no effect. GAS induced by PYY into the DMN was potentiated by coinjection of thyrotropin-releasing hormone (TRH, 30 ng) or the serotonin receptor (5-HT2) agonist (+/-)-1-(4-methyl-1-piperazinyl)-pyrrolo(1,2-a)quinoxaline (357 ng) and by microinjection of kainic acid (1 ng) into the raphe pallidus. Prepro-TRH-(160-169) (200 ng into the DMN) did not influence the stimulatory effect of PYY. PYY (200 ng) microinjected into the raphe pallidus, raphe obscurus, and nucleus ambiguous also increased GAS, although the response was of shorter duration than that in the DMN. These results indicate that PYY acts in brain stem nuclei involved in the vagal regulation of GAS and that PYY action in the DMN is potentiated by TRH or 5-HT2 receptor agonist acting at this site.

Effects of hCGRP I and II on gastric blood flow and acid secretion in anesthetized rabbits

1989 ◽  
Vol 256 (1) ◽  
pp. G145-G149 ◽  
Author(s):  
P. Bauerfeind ◽  
R. Hof ◽  
A. Hof ◽  
M. Cucala ◽  
S. Siegrist ◽  
...  
Keyword(s):  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Regional Blood Flow ◽  
Gastric Blood Flow ◽  
Human Calcitonin ◽  
Inverse Effect

Effects of intravenously administered human calcitonin gene-related peptides (hCGRP) I and II on regional blood flow and gastric acid secretion were examined in barbiturate-anesthetized rabbits. Blood flow was measured by injection of radioactively labeled microspheres at 0, 10, 20, 30, and 60 min. hCGRP I and II and vehicle were infused intravenously in five rabbits in rising doses of 0.01 (0-10th min), 0.03 (11-20th min), and 0.1 microgram.kg-1.min-1 (21-30th min). hCGRP I and II increased gastric blood flow dose dependently. Moreover, hCGRP I raised regional conductance (inverse of vascular resistance) in the stomach, duodenum, heart, brain, and skeletal muscle. As a result of the increased total peripheral conductance the mean arterial pressure was reduced, but the cardiac output remained unchanged. hCGRP II increased blood flow and conductance selectively in the stomach and the pancreas. The total peripheral conductance and mean arterial pressure remained unchanged. Apparently, hCGRP II exerts a more localized effect on the stomach than hCGRP I. hCGRP I and II did not affect basal gastric acid secretion. Pentagastrin-stimulated acid secretion was increased by 28% with hCGRP I (0.025 micrograms.kg-1.min-1) and decreased by 27% with hCGRP II (0.025 micrograms.kg-1.min-1). The inverse effect of hCGRP I and II and the parallel stimulation of blood flow brought about with hCGRP I and II indicate a different mode of action of the peptides on gastric blood flow and gastric acid secretion.

scholarly journals Intestinal fat-induced inhibition of meal-stimulated gastric acid secretion depends on CCK but not peptide YY

1999 ◽  
Vol 276 (2) ◽  
pp. G550-G555 ◽  
Author(s):  
Xiao-Tuan Zhao ◽  
John H. Walsh ◽  
Helen Wong ◽  
Lijie Wang ◽  
Henry C. Lin
Keyword(s):  
Small Intestine ◽  
Gastric Emptying ◽  
Acid Secretion ◽  
Receptor Antagonist ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Peptide Yy ◽  
Inhibitory Effect ◽  
Proximal Half

Fat in small intestine decreases meal-stimulated gastric acid secretion and slows gastric emptying. CCK is a mediator of this inhibitory effect (an enterogastrone). Because intravenously administered peptide YY (PYY) inhibits acid secretion, endogenous PYY released by fat may also be an enterogastrone. Four dogs were equipped with gastric, duodenal, and midgut fistulas. PYY antibody (anti-PYY) at a dose of 0.5 mg/kg or CCK-A receptor antagonist (devazepide) at a dose of 0.1 mg/kg was administered alone or in combination 10 min before the proximal half of the gut was perfused with 60 mM oleate or buffer. Acid secretion and gastric emptying were measured. We found that 1) peptone-induced gastric acid secretion was inhibited by intestinal fat ( P < 0.0001), 2) inhibition of acid secretion by intestinal fat was reversed by CCK-A receptor antagonist ( P < 0.0001) but not by anti-PYY, and 3) slowing of gastric emptying by fat was reversed by CCK-A antagonist ( P< 0.05) but not by anti-PYY. We concluded that inhibition of peptone meal-induced gastric acid secretion and slowing of gastric emptying by intestinal fat depended on CCK but not on circulating PYY.

Pancreatic polypeptide stimulates gastric acid secretion through a vagal mechanism in rats

1995 ◽  
Vol 269 (5) ◽  
pp. R983-R987 ◽  
Author(s):  
D. M. McTigue ◽  
R. C. Rogers
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Pancreatic Polypeptide ◽  
Acid Output ◽  
Arterial Infusion ◽  
Efferent Limb ◽  
Cervical Vagotomy ◽  
The Central Nervous System ◽  
Gastric Circulation

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.

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