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

scholarly journals Gastric acid secretion in uraemia and circulating levels of gastrin, somatostatin, and pancreatic polypeptide.

Gut ◽  
1979 ◽  
Vol 20 (9) ◽  
pp. 763-768 ◽  
Author(s):  
R Hallgren ◽  
J Landelius ◽  
K E Fjellstrom ◽  
G Lundqvist
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Pancreatic Polypeptide ◽  
Circulating Levels

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.

scholarly journals Effect of Individual L-Amino Acids on Gastric Acid Secretion and Serum Gastrin and Pancreatic Polypeptide Release in Humans

1982 ◽  
Vol 83 (1) ◽  
pp. 273-278 ◽  
Author(s):  
Ian L. Taylors ◽  
William J. Byrne ◽  
Dennis L. Christie ◽  
Marvin E. Ament ◽  
John H. Walsh
Keyword(s):  
Amino Acids ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Pancreatic Polypeptide ◽  
Serum Gastrin

Effect of hyperglycemia on gastric acid secretion during the gastric phase of digestion

1997 ◽  
Vol 272 (5) ◽  
pp. G1116-G1121 ◽  
Author(s):  
W. F. Lam ◽  
A. A. Masclee ◽  
E. S. Muller ◽  
C. B. Lamers
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Pancreatic Polypeptide ◽  
Acid Output ◽  
Serum Glucose ◽  
Phenol Red ◽  
Gastrin Release ◽  
Gastric Acid Output ◽  
Liquid Meal

We have examined the effect of an acute stable hyperglycemia on gastric acid secretion during the gastric phase of digestion. Gastric acid output was measured with a recovery marker (phenol red) under basal conditions and after repeated intragastric instillation of a liquid meal in seven healthy subjects on two separate occasions: during normoglycemia (serum glucose, 15 mM). Premeal gastric acid output was significantly (P < 0.05) reduced during hyperglycemia compared with during normoglycemia (2.6 +/- 1.0 vs. 5.8 +/- 1.8 mmol/h). Intragastric meal-stimulated incremental acid output during hyperglycemia was significantly (P < 0.05) reduced compared with during normoglycemia (19 +/- 4 vs. 38 +/- 9 mmol/120 min). Meal-stimulated gastrin release during hyperglycemia was significantly (P < 0.05) reduced compared with that during normoglycemia (4.9 +/- 1.3 vs. 6.6 +/- 1.6 micrograms.1(-1).120 min-1). The intragastric meal induced significant (P < 0.05) increases in pancreatic polypeptide concentrations only during normoglycemia. During hyperglycemia, recovery rates of gastric contents were significantly (P < 0.05) increased compared with during normoglycemia, both before (81 +/- 4 vs. 71 +/- 6%) and after (72 +/- 4 vs. 57 +/- 4%) meal ingestion, pointing to delayed gastric emptying of liquids during hyperglycemia. In conclusion, 1) gastric acid secretion under unstimulated conditions and during the gastric phase of digestion is reduced during hyperglycemia; 2) meal-stimulated gastrin release is significantly reduced during hyperglycemia; 3) the reduction in meal-stimulated acid output is correlated with the reduction in gastrin releases; and 4) pancreatic polypeptide secretion is significantly reduced during hyperglycemia, pointing to impaired vagal cholinergic tone.

Role of pancreatic polypeptide in canine gastric acid secretion.

1979 ◽  
Vol 236 (4) ◽  
pp. E488 ◽  
Author(s):  
D L Parks ◽  
R L Gingerich ◽  
B M Jaffe ◽  
B Akande
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Significant Role ◽  
Pancreatic Polypeptide ◽  
Gastric Fistula ◽  
Background Infusion ◽  
Duodenal Acidification ◽  
Acid Release

The interrelationships of canine pancreatic polypeptide (cPP) and gastric acid secretion were studied in dogs following infusion of histamine or pentagastrin. Pentagastrin stimulated gastric acid release 30-fold and simultaneously increased plasma cPP secretion by an average of 120 pg/ml. Although histamine stimulated gastric acid secretion to a comparable degree, it had no effect on plasma cPP levels. Three mechanisms of inhibition of acid secretion (cimetidine, duodenal acidification, and somatostatin) had different effects on pancreatic polypeptide (PP) levels. With a background infusion of pentagastrin, cimetidine did not affect cPP levels. In contrast, somatostatin dramatically inhibited both gastric fistula output and cPP release. Finally, a 10-min duodenal irrigation with 0.1 N HCl resulted in a brief spike in cPP levels (from 266 +/- 12 to 347 +/- 31 pg/ml) at the time of greatest inhibition of histamine-stimulated acid secretion. Infusions of histamine + porcine pancreatic polypeptide (pPP) at concentrations of 1.0 and 2.25 microgram/kg per h and of pentagastrin + pPP at 2.25 microgram/kg per h closely simulated postprandial cPP levels (mean 1306 +/- 18 pg/ml at 30 min) but produced no change in gastric fistula output. These studies demonstrated that PP levels and rates of gastric acid secretion are unrelated and that at physiologic concentrations PP plays no significant role in the regulation of gastric acid secretion.

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