Canine bombesin‐like gastrin releasing peptides stimulate gastrin release and acid secretion in the dog.

Bunnett, Nigel W.; Clark, Brian R.; Debas, Haile T.; Milton, Roy C.; Kovacs, Thomas O.; Orloff, Mark S.; Pappas, Theodore N.; Reeve, Joseph R.; Rivier, Jean; Walsh, John H.

doi:10.1113/jphysiol.1985.sp015762

Cited by 28 publications

(8 citation statements)

References 19 publications

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“…Therefore, EGF may stimulate gastrin gene expression in addition to its role as a luminal growth factor. Antral G cells are also stimulated by neuropeptides released from antral nerves, such as gastrin-releasing peptide (GRP) (10,11) and vasoactive intestinal peptide (VIP) (4). Although studies ofisolated G cells show that GRP stimulates gastrin secretion (12,13), the effect of GRP on gastrin gene expression has not been reported.…”

Section: Introductionmentioning

confidence: 99%

Regulation of the gastrin promoter by epidermal growth factor and neuropeptides.

Godley

Brand

1989

Proc. Natl. Acad. Sci. U.S.A.

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The regulation of gastrin gene transcription was studied in GH4 pituitary cells transfected with constructs comprised of the first exon of the human gastrin gene and various lengths of 5' regulatory sequences ligated upstream of the reporter gene chloramphenicol acetyltransferase. Gastrin reporter gene activity in GH4 cells was equal to the activity of a reporter gene transcribed from the endogenously expressed growth hormone promoter. The effect of a variety of peptides on gastrin gene transcription including epidermal growth factor (normally present in the gastric lumen), gastrinreleasing peptide, vasoactive intestinal peptide, and somatostatin (present in gastric nerves) was assessed. Epidermal growth factor increased the rate of gastrin transcription almost 3-fold, whereas thyrotropin-releasing hormone and vasoactive intestinal peptide increased gastrin transcription 2-and 1.5-fold, respectively. Gastrin-releasing peptide, a peptide that strongly stimulates gastrin release, weakly increased gastrin transcription (1.3-fold). Somatostatin inhibited the increase in gastrin transcription induced by epidermal growth factor, thyrotropin-releasing hormone, and vasoactive intestinal peptide. Constructs containing various lengths of 5' regulatory sequences defmed a response element -40 to -82 base pairs (bp) 5' to the transcription initiation site. This 40-bp sequence contains Spl and AP2 binding sites, which suggests that epidermal growth factor and thyrotropin-releasing hormone stimulate gastrin gene transcription through transcription factors that bind to Spl and/or AP2 motifs.

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Section: Introductionmentioning

confidence: 99%

Regulation of the gastrin promoter by epidermal growth factor and neuropeptides.

Godley

Brand

1989

Proc. Natl. Acad. Sci. U.S.A.

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“…in enteric nerves that control gastrin secretion, were incubated with the GRP antibody used for neurochemical coding (goat) and a well-characterized antibody that was raised in rabbits (45). Both antibodies stained the same DRG neurons, and both stained neurons of the myenteric plexus and mucosal nerve fibers of the gastric antrum (Supplemental Figure 1; supplemental material available online with this article; doi:10.1172/JCI64551DS1).…”

Section: Tgr5 Is Expressed By Peptidergic Neurons Of the Drgmentioning

confidence: 99%

The TGR5 receptor mediates bile acid–induced itch and analgesia

et al. 2013

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Patients with cholestatic disease exhibit pruritus and analgesia, but the mechanisms underlying these symptoms are unknown. We report that bile acids, which are elevated in the circulation and tissues during cholestasis, cause itch and analgesia by activating the GPCR TGR5. TGR5 was detected in peptidergic neurons of mouse dorsal root ganglia and spinal cord that transmit itch and pain, and in dermal macrophages that contain opioids. Bile acids and a TGR5-selective agonist induced hyperexcitability of dorsal root ganglia neurons and stimulated the release of the itch and analgesia transmitters gastrin-releasing peptide and leucineenkephalin. Intradermal injection of bile acids and a TGR5-selective agonist stimulated scratching behavior by gastrin-releasing peptide-and opioid-dependent mechanisms in mice. Scratching was attenuated in Tgr5-KO mice but exacerbated in Tgr5-Tg mice (overexpressing mouse TGR5), which exhibited spontaneous pruritus. Intraplantar and intrathecal injection of bile acids caused analgesia to mechanical stimulation of the paw by an opioid-dependent mechanism. Both peripheral and central mechanisms of analgesia were absent from Tgr5-KO mice. Thus, bile acids activate TGR5 on sensory nerves, stimulating the release of neuropeptides in the spinal cord that transmit itch and analgesia. These mechanisms could contribute to pruritus and painless jaundice that occur during cholestatic liver diseases.

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“…Bunnet et al (29) demonstrated that neuromedin C stimulated gastrin release and gastric acid secretion in conscious dogs with gastric cannulae. This suggested that the mechanism via gastric acid secretion also had a stimulatory effect on the pancreas.…”

Section: Discussionmentioning

confidence: 98%

Mechanisms of Stimulatory Effect of Neuromedin C on Pancreatic Exocrine Secretion in Conscious Rats

Okubo

Miyasaka

Matsumoto³

et al. 1994

Pancreas

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The mechanisms of the stimulatory effect of the bombesin-like peptide neuromedin C on pancreatic exocrine secretion were examined in conscious rats. Rats were prepared with cannulae draining bile and pancreatic juice separately. Intravenous infusion of 0.35 nmoykg/h of neuromedin C significantly increased the secretions of pancreatic bicarbonate and protein, and transiently increased the plasma cholecystokinin (CCK) concentration. The increase in pancreatic secretion persisted for 90 min, whereas the increase in plasma CCK was observed only after 15 and 30 min from the beginning of neuromedin C infusion. Intravenous infusion of CR-1409, a specific CCK-receptor antagonist, inhibited, but did not abolish, the protein secretion stimulated by neuromedin C. Intraduodenal infusion of a potent proton pump inhibitor, omeprazole, suppressed, but did not abolish, protein secretion induced by neuromedin C. Omeprazole abolished the increase in bicarbonate secretion produced by neuromedin C. These results indicate that neuromedin C induces release of CCK and that its induction of pancreatic hypersecretion is due to both its direct effect and CCK. The results also suggest that gastric hypersecretion may have a role in the bicarbonate hypersecretion induced by neuromedin C.

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Canine bombesin‐like gastrin releasing peptides stimulate gastrin release and acid secretion in the dog.

Cited by 28 publications

References 19 publications

Regulation of the gastrin promoter by epidermal growth factor and neuropeptides.

Regulation of the gastrin promoter by epidermal growth factor and neuropeptides.

The TGR5 receptor mediates bile acid–induced itch and analgesia

Mechanisms of Stimulatory Effect of Neuromedin C on Pancreatic Exocrine Secretion in Conscious Rats

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