Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gastrin-releasing peptide (GRP) and bombesin can stimulate pepsinogen release by both gastrin-dependent and -independent mechanisms. Using isolated guinea pig gastric chief cells, we determined that GRP can act directly on the guinea pig chief cell to cause pepsinogen release. GRP and bombesin stimulated a 2.5- to 3-fold increase in pepsinogen release above basal release. Substance P also stimulated a small but significant increase in pepsinogen release. No gastrin immunoreactivity was detected in the supernatants of cells stimulated with up to 1 microM GRP or bombesin or 1 mM carbachol. GRP-stimulated pepsinogen release was completely inhibited by GRP/bombesin receptor agonists as well as substance P receptor antagonist but not by antagonists to receptors for gastrin, the octapeptide of cholecystokinin (CCK-8), secretin, vasoactive intestinal peptide (VIP), or muscarinic agents. Substance P-stimulated pepsinogen release was completely inhibited by substance P receptor antagonist but not by GRP/bombesin receptor antagonists. An additive effect on pepsinogen release was seen when GRP was combined with maximally effective concentrations of adenosine 3',5'-cyclic monophosphate (cAMP)-mediated agents (VIP, secretin, 8-BrcAMP) but not with calcium-mediated agents (carbachol, CCK-8, gastrin). These results indicate that GRP can directly stimulate pepsinogen release from guinea pig chief cells by a specific GRP receptor that mobilizes intracellular calcium.
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PMID:Gastrin-releasing peptide directly releases pepsinogen from guinea pig chief cells. 170 Jun 25

The levels of 10 regulatory peptides in acid-alcohol extracts of three regions of the small intestine (0-20%, 30-60%, and 70-100%, with respect to distance from the pylorus) have been monitored radioimmunometrically in sham-infected male (6-8 week old) C57 mice and mice given a 5-cysticercoid infection of the rat tapeworm Hymenolepis diminuta and autopsied 10 days postprimary infection and 5 days postsecondary infection (administered 28 days postprimary infection). The regulatory peptides examined were gastrin, gastrin-releasing peptide (GRP), glucagon (= enteroglucagon), motilin, neurotensin (NT), pancreatic polypeptide (PP), peptide histidine isoleucine (PHI), somatostatin (SRIF), substance P (SP), and vasoactive intestinal peptide (VIP). Statistical analyses revealed significant deviations from control values of five of the peptides (enteroglucagon and SP, both elevated; NT, PHI and VIP, all lowered) in intestinal tissue from infected mice; measurement of the same peptides in colonic extracts revealed no significant differences between infected and sham-infected mice. Parallel changes in peptide levels between normal infected and immunosuppressed infected mice were not evident, although elevations in the tissue levels of enteroglucagon and SP were found in infected Wistar rats (normal host). Results are discussed with respect to a peptidergic involvement in the pathology and host immune response to an intestinal tapeworm.
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PMID:Hymenolepis diminuta: changes in the levels of certain intestinal regulatory peptides in infected C57 mice. 171 77

The fasting plasma levels of 9 gastrointestinal regulatory peptides were measured by radioimmunoassay in 13 stable patients with chronic renal failure receiving hemodialysis treatment regularly and compared with those of 10 healthy controls. The plasma concentrations of gastrin-releasing peptide, motilin, neurotensin, pancreatic polypeptide, peptide YY, somatostatin, substance P, and vasoactive intestinal peptide were increased. The plasma level of gastrin was not statistically different from that of the controls (p = 0.077). We conclude that patients with chronic renal failure receiving hemodialysis treatment regularly have increased concentrations of eight of nine measured gastrointestinal regulatory peptides. The elevated levels of gastrointestinal peptides in patients with chronic renal failure may contribute to uremic gastrointestinal symptoms and dysfunctions. It is necessary to make a renal function evaluation before interpreting measured plasma levels of gastrointestinal regulatory peptides.
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PMID:Plasma levels of gastrointestinal regulatory peptides in patients receiving maintenance hemodialysis. 171 7

Gastric acidity is influenced by systemic and local peptide effects. Previous work by others has shown that intraluminally secreted peptides may have a role in local control of gastric acidity; however, the response of these peptides to acute changes in gastric pH is unknown. To determine the effects of acute changes in pH on systemic and intraluminal peptide levels, 14 normal volunteers underwent placement of a nasogastric tube after an overnight fast. Blood and gastric fluid were analyzed on a control day, 2 hours after completion of 24 hours of aluminum-magnesium antacid therapy and after 24 hours of H2 blockade. Plasma and acid-alcohol-extracted gastric peptide levels were measured with specific radioimmunoassays. Specimens were subdivided into two groups: 28 gastric fluid specimens with a pH less than 4 and 10 specimens with a pH greater than 4. In the patients with a pH greater than 4, the luminal peptides, motilin, neurotensin, pancreatic polypeptide, somatostatin, substance P, and gastrin, were decreased by 50% to 90% and gastrin-releasing peptide was decreased by 36% compared with specimens with a pH less than 4. Conversely, intraluminal vasoactive intestinal polypeptide and calcitonin levels were elevated by 60% and 27%, respectively, in the samples with a pH greater than 4. Intraluminal peptide concentrations are responsive to changes in intragastric pH; however, this response was not seen in plasma peptide levels.
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PMID:Acute gastric pH changes alter intraluminal but not plasma peptide levels. 172 Sep 3

This study performed on 6 conscious cats with chronic pancreatic fistulas was designed to determine the role of cholecystokinin (CCK), gastrin and gastrin-releasing peptide (GRP) in stimulation of pancreatic secretion in this species. Pancreatic response to GRP infused intravenously in graded doses appears to be mediated predominantly by CCK because a CCK receptor antagonist, L-364,718, abolished this response. Also, gastrin appears to mediate in part the secretory response to GRP because blockade of gastrin receptors by L-365,260, given at the dose that completely abolished the pancreatic response to exogenous gastrin, caused a significant reduction in the bombesin-induced pancreatic secretion. CCK and partly gastrin appear to mediate the postprandial pancreatic secretion in cats as the administration of L-364,718 and L-365,260 inhibited this secretion by over 90 and 30%, respectively. In contrast, GRP does not seem to contribute to food-induced pancreatic secretory stimulation, because the blockade of GRP receptors using novel bombesin/GRP antagonist (RC-3100) failed to affect this secretion. We conclude that CCK and partly gastrin, but not GRP, play an essential role in the postprandial pancreatic secretion.
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PMID:Role of cholecystokinin, gastrin and gastrin-releasing peptide in the regulation of pancreatic secretion in cats. 172 67

The effect of sepsis on plasma levels of various gut peptides was studied in rats. Sepsis was induced by cecal ligation and puncture (CLP); control animals underwent sham operation. Sixteen hours after CLP or sham operation, portal and systemic blood was drawn, and plasma levels of gastrin, vasoactive intestinal peptide (VIP), secretin, peptide YY (PYY), gastrin-releasing peptide (GRP), and substance P were determined by radioimmunoassay. Plasma levels of gastrin, VIP, PYY, and secretin were elevated in septic rats compared with nonseptic animals, with the highest levels noted in portal blood. There was no effect of sepsis on GRP or substance P levels. In other experiments, human recombinant interleukin 1 alpha (IL-1 alpha) or recombinant tumor necrosis factor alpha (TNF alpha) was injected intraperitoneally (300 micrograms/kg body weight in 3 divided doses over 16 hours). There was no change in plasma levels of gut peptides after IL-1 alpha injection. TNF alpha induced elevation of PYY levels in portal plasma with no change in other gut peptide levels. The results suggest that sepsis stimulates release of certain gut peptides and that TNF, but not IL-1, may be partly responsible for this response. The mechanism of the release of gut peptides and its significance in the pathophysiologic changes induced by sepsis remain to be determined.
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PMID:Effect of sepsis or cytokine administration on release of gut peptides. 173 67

The serum gastrin response to an infusion of gastrin-releasing peptide (GRP), with or without simultaneous fundic distension, was studied in healthy volunteers and in patients with duodenal ulcer disease before and after a complete proximal gastric vagotomy (PGV). We also studied the effect of fundic distension alone on gastrin release and intraluminal gastric pressure in healthy volunteers and in patients after PGV. We observed an increased intraluminal pressure in patients after PGV compared with healthy subjects. During fundic distension with 600 ml of air no significant increase in gastrin values was observed in healthy subjects or in duodenal ulcer patients. In healthy subjects fundic distension significantly inhibited the gastrin response to the higher dose of GRP. This inhibitory effect exerted by fundic distension was counteracted by cholinergic blockade. In contrast, fundic distension did not alter the gastrin response to GRP in duodenal ulcer patients, suggesting a defective inhibitory mechanism in duodenal ulcer patients. After PGV, GRP infusion resulted in an enhanced gastrin response, and fundic distension seemed to facilitate the gastrin-stimulatory effect of GRP. This supports the concept of a vagally dependent inhibitory oxyntopyloric mechanism and that fundic distension can elicit both inhibitory and stimulatory secretory mechanisms.
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PMID:Inhibition of gastrin release induced by fundic distension. Evidence of a defective inhibition in duodenal ulcer patients. 176 93

Gastrin-releasing peptide (GRP) was infused in graded doses (1-27 pmol/kg per h) to healthy human volunteers to study the effects on gastric, pancreatic and gallbladder functions as well as on gastrin, CCK and PP release. The results were compared to equimolar doses of synthetic bombesin. GRP significantly (P less than 0.05) stimulated gastric and pancreatic secretory responses, gallbladder contraction and gastro-enteropancreatic hormone release in a dose-dependent manner. GRP was found to be equipotent to bombesin with respect to gastric acid secretion, pancreatic enzyme output, gallbladder contraction and plasma hormone release. We conclude (a) that human GRP has similar biologic effects as synthetic bombesin; (b) as GRP is localized exclusively in nerve tissue and has potent effects on different organs, it is a likely candidate for peptidergic control of human gastric, pancreatic and gallbladder functions.
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PMID:Human gastrin-releasing peptide: biological potency in humans. 181 Dec 76

Endocrine cells in the acid-secreting part of the avian stomach, the proventriculus, contain two forms of gastrin-releasing peptide (GRP) of 27 and 6 residues, respectively. We have examined the actions of exogenous GRP-27 and GRP-6 and endogenously released GRP in the control of pancreatic secretion in urethan-anesthetized turkeys. Chicken GRP-27 and the structurally related amphibian peptide bombesin were potent stimulants of fluid and protein output from the pancreas (at 6-100 pmol/kg, iv). GRP-6 had no significant effect at doses up to 1,000 times higher. A bombesin antagonist, (CH3)2-CHCO-[D-Ala24]GRP-20--26-NHCH3, inhibited the action of exogenous chicken GRP-27 but did not inhibit intravenous cholecystokinin octapeptide (CCK-8). Distension of the proventriculus with a solution of peptone produced an increase in the flow of pancreatic juice and an increase in protein output, which was not reduced by atropine. The bombesin antagonist produced a reversible inhibition of this response. A CCK-gastrin antagonist, BOC-beta-Ala-Trp-Leu-Asp-O(CH2)2- phenyl(4F), which inhibited the action of exogenous CCK, had no effect on the pancreatic response to exogenous GRP-27 or to distension of the proventriculus with peptone. We suggest that protein-rich solutions in the proventriculus release GRP, which in turn acts directly on the pancreas to stimulate enzyme secretion.
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PMID:Hormonal control of avian pancreas by gastrin-releasing peptide from the proventriculus. 185 84

Addition of gastrin releasing peptide to serum-starved Swiss 3T3 mouse fibroblasts results in a transient appearance of a myelin basic protein-kinase activity in cytosolic extracts. Increased kinase activity is also observed upon stimulation of cells with bradykinin, epidermal growth factor or 4 beta-phorbol dibutyrate. Chromatographic analysis of the cytosolic extracts show that both gastrin-releasing peptide and 4 beta-phorbol dibutyrate induce the appearance of a kinase activity similar to that induced by epidermal growth factor. The response to gastrin-releasing peptide is abolished by down-regulation of protein kinase C and attenuated by acute inhibition of protein kinase C using staurosporine. The effect of epidermal growth factor was also suppressed under these conditions, albeit to a lesser extent. The results indicate (1) that activation of myelin basic protein kinase(s) may be common to different growth factors, and (2) that protein kinase C may participate in this response, at least in the case of gastrin-releasing peptide.
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PMID:Protein kinase C-dependent activation of a myelin basic protein kinase by gastrin-releasing peptide in Swiss 3T3 fibroblasts. 193 82


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