The effect of somatostatin and 16,16-dimethyl-prostaglandin E2 on bombesin-stimulated canine gastric acid, plasma gastrin and pancreatic polypeptide secretion.
We studied the effect of the intravenous infusion of 16,16-dimethylprostaglandin E2 methyl ester (di-M-PGE2) and somatostatin on bombesin-stimulated gastric acid secretion, plasma gastrin and plasma pancreatic polypeptide in four chronic gastric fistula dogs. Bombesin-stimulated gastric acid secretion was significantly inhibited by somatostatin and virtually abolished by di-M-PGE2. Both agents caused significant, but indistinguishable inhibition of gastrin release (P less than 0.05). Bombesin-stimulated pancreatic polypeptide release was also significantly inhibited by both somatostatin and di-M-PGE2; the inhibitory effect of somatostatin was significantly greater than that of di-M-PGE2 (P less than 0.05). This study provides further evidence in support of the complex interrelationships between agents responsible for the modulation of gastrointestinal physiology.
D015064:16,16-Dimethylprostaglandin E2 / Q000494:pharmacology*; D000818:Animals; D001839:Bombesin / Q000494:pharmacology*; D004285:Dogs; D005744:Gastric Acid / Q000378:metabolism*; D005755:Gastrins / Q000378:metabolism*; D007700:Kinetics; D010191:Pancreatic Polypeptide / Q000378:metabolism*; D010455:Peptides / Q000494:pharmacology*; D011459:Prostaglandins E, Synthetic / Q000494:pharmacology*; D013004:Somatostatin / Q000494:pharmacology*
D005755:Gastrins; D010455:Peptides; D011459:Prostaglandins E, Synthetic; D013004:Somatostatin; D010191:Pancreatic Polypeptide; D015064:16,16-Dimethylprostaglandin E2; D001839:Bombesin