gastrin-releasing-peptide and Gastric-Fistula

Gastrin-releasing peptide (GRP) has a wide range of biological actions, including stimulation of the frequency of antral contractions and delaying gastric emptying. The present study was designed to evaluate the role of GRP in the control of gastric emptying of liquid test meals in the rat. The emptying of methyl cellulose given by gavage to fasted rats, or of saline given via the fistula to conscious gastric fistula rats was not influenced by the GRP antagonists, NC-8-89 (Leu13-psi-(CH2NH)-Leu14-bombesin) and 2258U89 ((de-NH2)Phe19, D-Ala24, D-Pro26 psi (CH2NH)Phe27(-GRP (19-27)), at 2 mg/kg, s.c. However, both antagonists (0.02, 0.2 and 2 mg/kg) reversed the inhibitory effect of HCI on gastric emptying in gastric fistula rats (P < 0.05-0.001). When peptone was administered after a preload, but not otherwise, the inhibition of emptying was also partly reversed by both antagonists at all doses used (P < 0.05-0.001). Interestingly, the delay in the emptying of hyperosmolal saline compared to saline, was enhanced at a dose of 0.2 mg/kg of both antagonists (P < 0.05 and P < 0.01). Food intake did not change significantly with the two lower doses of antagonists, but was decreased by the highest dose of NC 8-89. We conclude that GRP specifically inhibits gastric emptying of acid and peptone solutions in the conscious rat.

Topics: Animals; Bombesin; Dose-Response Relationship, Drug; Eating; Gastric Emptying; Gastric Fistula; Gastrin-Releasing Peptide; Male; Methylcellulose; Peptides; Rats; Rats, Sprague-Dawley

Bombesin (BN) and its mammalian relatives, gastrin-releasing peptide (GRP) and neuromedin B (NMB), have been implicated in the control of food intake, and more recently systemic injections of BN have been shown to suppress need-free and sodium deficiency-induced salt (NaCl) intake. Postoral mechanisms that are activated by the ingestion of salt contribute to the termination of salt intake. The hypothesis that BN-like peptides potentiate postoral salt ingestion-contingent feedback and thereby accelerate the termination of salt intake was evaluated by measuring the effects of peripheral injections of BN (4, 6, 16 micrograms/kg), GRP (4, 8, 16 micrograms/kg), and NMB (4, 8, 16 micrograms/kg) on sham (gastric fistula open) and normal (gastric fistula closed) drinking of NaCl (0.5 M) by sodium-deficient male rats. Sodium deficiency was induced by injections of deoxy-corticosterone acetate and furosemide. Injections of 4 micrograms/kg BN produced a transient suppression in the sham drinking of salt and a more sustained reduction of salt intake when postoral factors were present in the normal drinking condition. In contrast, injections of 6 and 16 micrograms/kg BN produced the same pronounced suppression in salt intake in both the closed and open fistula test conditions. Only 16 micrograms/kg GRP was behaviorally effective, and this des: reliably suppressed both normal and sham drinking of salt. On an equimolar basis, BN was more potent than GRP. Injections of NMB had no effect on salt intake under any dose or fistula condition. The order of BN-like peptide potency in suppressing sham and normal drinking of salt by sodium-deficient rats (BN > GRP > NMB) is similar to the peptides' effects on feeding. When postoral feedback is minimized, the combination of BN or GRP and pregastric stimuli mimic the salt intake by rats in the fistula closed, normal drinking condition.

Topics: Animals; Bombesin; Dose-Response Relationship, Drug; Eating; Feeding Behavior; Gastric Fistula; Gastrin-Releasing Peptide; Male; Neurokinin B; Peptides; Rats; Rats, Sprague-Dawley; Sodium; Sodium Chloride, Dietary

The mammalian counterpart to bombesin, gastrin-releasing peptide (GRP), is considered to stimulate gastric acid secretion by release of endogenous gastrin. The present study was carried out to examine if GRP has a stimulatory action on acid secretion in addition to that produced by released gastrin. In 4 gastric fistula (GF) and Heidenhain pouch (HP) cats, 160 pmol X kg-1 X h-1 i.v. GRP produced a GF and HP acid response that amounted to 22 and 13%, respectively, of the maximal acid response to pentagastrin, with no rise in serum gastrin concentration. GRP significantly increased the maximal acid response to pentagastrin in the GF but not in the HP. These results suggest that GRP stimulates acid secretion in cats also by an action not related to the release of gastrin. This action is greater in the presence of vagal innervation.

Topics: Animals; Cats; Gastric Acid; Gastric Fistula; Gastrin-Releasing Peptide; Gastrins; Pentagastrin; Peptides; Vagotomy

Topics: Animals; Cholecystokinin; Consciousness; Dogs; Dose-Response Relationship, Drug; Gastric Fistula; Gastrin-Releasing Peptide; Pancreas; Pancreatic Fistula; Pancreatic Juice; Pancreatic Polypeptide; Peptides; Stimulation, Chemical