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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent investigations have shown that the functions of the gastrointestinal organs may be regulated by a complex system of paracrine cells and peptidergic nerves, in addition to the established humoral and autonomic nervous systems. In this article we discuss the possible paracrine regulation of the secretory functions of the stomach and the pancreas by somatostatin-producing D-cells. Secondly, we discuss the distribution, localization, effects and secretion of the neuropeptides VIP and 'gastrin-releasing polypeptide' (GRP or 'mammalian bombesin') applied to the stomach (GRP) and pancreas (GRP and VIP) of the pig. It is concluded, that all three peptides are capable of influencing powerfully the secretory state of these organs, and that these newer regulatory peptides probably play an important role in the integrate neurohormonal control of gastrointestinal secretion.
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PMID:Interrelation of nerves and hormones in stomach and pancreas. 613 53

Weak to strong gastrin releasing peptide--bombesin (GRP-Bn)-like immunoreactivity was found in fine varicose nerve terminal systems of low to high densities in several parts of the CNS. The highest densities of strongly immunoreactive terminals were found in the marginal layer and in the substantia gelatinosa of the spinal cord, and in parts of the nuc. tractus spinalis nervi trigemini. Morphometrical analysis in the spinal cord demonstrates that GRP-BN-like-immunoreactive and substance P (SP), but not somatostatin (SS)-immunoreactive nerve terminals strikingly codistribute. Coexistence of SP and GRP-BN-like immunoreactivities was demonstrated in trigeminal and spinal ganglion nerve cells. Thus, GRP-BN-like immunoreactivity may coexist with SP in certain SP-immunoreactive nerve terminal systems.
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PMID:Immunohistochemical indications of gastrin releasing peptide--bombesin-like immunoreactivity in the nervous system of the rat. Codistribution with substance P-like immunoreactive nerve terminal systems and coexistence with substance P-like immunoreactivity in dorsal root ganglion cell bodies. 619 65

The effect of intravenous administration of gastrin-releasing peptide ( GRP ) on serum gastrin and insulin levels was studied in ad libitum fed and 24-h fasted rats. Administration of GRP (55 micrograms/kg body weight) caused a significant (P less than 0.05) elevation in serum gastrin levels at 10, 30, 60, and 120 min in the rats fed ad libitum, whereas in the fasted rats, gastrin levels rose significantly only at 10 min. GRP did not cause insulin release in fasted rats, but in the fed rats, it led to a significant elevation in serum insulin levels at 10 and 30 min, in comparison to controls. GRP appears to have an insulinotropic action in addition to a gastrin-releasing effect.
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PMID:Insulinotropic and gastrin-releasing action of gastrin-releasing peptide (GRP). 637 71

The effect of GRP on the in vivo canine antrum was investigated. GRP caused a dose-dependent increase in antral gastrin output which was not significantly altered by administration of tetrodotoxin. The higher doses of GRP administered also caused excitation of antral motility which was abolished by tetrodotoxin, a finding in contrast to previous in vitro results demonstrating bombesin-induced antral smooth muscle contraction to be tetrodotoxin-resistant. These data suggest that in the in vivo canine model GRP causes antral gastrin release via non-neurally mediated mechanisms (probably by acting directly on the G-cell) and excites antral motility via neurally-mediated mechanisms.
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PMID:Effects of porcine gastrin releasing peptide (GRP) on canine antral motility and gastrin release in vivo. 648 63

The heptacosapeptide amide corresponding to the entire amino acid sequence of chicken gastrin-releasing peptide (cGRP) was synthesized similarly to the synthesis of porcine GRP by assembling six peptide fragments followed by deprotection with 1 M trifluoromethanesulfonic acid-thioanisole in TFA. A new carboxyl-activating reagent, thiazolidine-2-thione, was preferentially adopted for preparation of necessary fragments. The synthetic cGRP, purified by ion-exchange chromatography, followed by partition chromatography, was active as the synthetic porcine GRP, when plasma immunoreactive gastrin level was examined in rats. No obvious difference was observed when synthetic and natural cGRP preparations were compared by HPLC, immunochemical property and biological activity in dogs.
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PMID:Studies on peptides. CXI. Synthesis of chicken gastrin-releasing peptide. 712 60

Using AR4-2J rat pancreatic carcinoma cells, the effects of a novel bombesin (BN) receptor antagonist [D-F5Phe6, D-Ala11]BN(6-13)OMe (BIM26226) on BN- or GRP-stimulated amylase release and binding of radio-labeled bombesin-like peptides to these cells were examined and compared to [D-Phe6,Leu13 psi(CH2NH)Leu14]BN(6-14) (Psi Bn(6-14)), one of the most potent BN receptor antagonists presently known. BN and GRP both stimulated amylase release with EC50 values in the nanomolar range. Both antagonists were devoid of agonist activity when tested alone. BIM26226 was most potent, antagonizing BN- or GRP-stimulated amylase release with IC50 values in the nanomolar range, whereas Psi Bn(6-14) was approximately ten times less potent. With 125I-[Tyr15]GRP bound to these cells, the binding affinities were BIM26226 > GRP > Psi Bn(6-14) >> neuromedin B. BIM 22626 was not able to inhibit binding of radio-labeled CCK-33, gastrin-17 or VIP. These results suggest that BIM26226 is one of the most potent and specific bombesin receptor antagonists in vitro and seems to be a useful tool to define the physiologic role of GRP in vivo.
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PMID:Effects of BIM26226, a potent and specific bombesin receptor antagonist, on amylase release and binding of bombesin-like peptides to AR4-2J cells. 753 56

Ionophoresis of the smaller bombesin-like peptides (gastrin releasing peptide [GRP]-(18-27), neuromedin B, and bombesin) evoked responses from 30-60% of hamster suprachiasmatic nucleus cells recorded in a hypothalamic slice preparation, depending on the circadian phase. We also demonstrated for the first time that the putative bombesin-like peptide receptor antagonists [D-F5,D-Phe6,D-Ala11]bombesin-(6-13)methyl ester (BIM 26226) and [D-Phe6,Des-Met14]bombesin-(6-14)ethyl amide can be applied ionophoretically to block physiological responses to bombesin-like peptides. Together with earlier findings, these results show that bombesin-like peptides administered by several methods can potently alter the firing rates of hamster suprachiasmatic nucleus neurons in vitro. These results indicate that bombesin-like peptides affect suprachiasmatic nucleus cells and could play a role in modulating suprachiasmatic nucleus-mediated circadian rhythm entrainment.
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PMID:Effects of ionophoretically applied bombesin-like peptides on hamster suprachiasmatic nucleus neurons in vitro. 770 41

The aim of the present study was to evaluate the effect of the opiate receptor antagonist naloxone on vagally stimulated secretion of bombesin-like immunoreactivity (BLI), somatostatin and gastrin from the isolated rat stomach, which was perfused via the celiac artery with Krebs-Ringer buffer. Vagal stimulation was performed for 10 min with 1 ms, 10 V and 2, 5, 10 or 20 Hz, respectively. In control experiments BLI release increased significantly above basal secretion during a stimulation frequency of 10 Hz (1367 +/- 357 pg/10 min; P < 0.001) and 20 Hz (996 +/- 202 pg/10 min; P < 0.01), but not at 2 and 5 Hz. In comparison to the controls naloxone (10(-6) M) significantly increased BLI secretion at 5 Hz by 573 +/- 150 pg/10 min (P < 0.05), but attenuated the BLI response to higher stimulation frequencies of 10 and 20 Hz to 284 +/- 143 pg/10 min (P < 0.001) and 490 +/- 114 pg/10 min (P < 0.01), respectively. At 2 Hz naloxone had no effect on BLI release. As shown previously the cholinergic blocker atropine (10(-7) M) induced a significant BLI release during vagal stimulation at 2 Hz (680 +/- 233 pg/10 min; P < 0.01) and 5 Hz (935 +/- 324 pg/10 min; P < 0.05), but was without effect at 10 and 20 Hz compared to the controls. The effects of the combination of naloxone and atropine were similar to naloxone and atropine alone. Naloxone had no effect on vagal or GRP-induced regulation of gastrin and somatostatin release.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of endogenous opioids on vagally induced release of gastrin, somatostatin and bombesin-like immunoreactivity from the perfused rat stomach. 775 6

Chicken gastrin has a C-terminal sequence resembling mammalian cholecystokinin, but its biological properties resemble mammalian gastrin. The mechanisms controlling chicken gastrin release are poorly understood. We have investigated the factors which influence chicken gastrin secretion in vivo. Plasma gastrin concentration was decreased within 12 h of fasting, but tissue gastrin concentrations were not significantly changed even after 24 h of food deprivation. In birds fasted for 24 h and treated with the H+/K(+)-ATPase inhibitor, omeprazole, plasma gastrin concentration was greatly enhanced indicating the importance of acid inhibition of the gastrin cell. It is well established that amino acids (particularly aromatics like Phe and Trp) and peptides stimulate gastrin release in mammals. In chicken, however, Met, His and Arg were the strongest stimulant amongst the essential amino acids investigated. Of these three amino acids, Met rapidly stimulated gastrin release. The GRP antagonist M216140 did not suppress the Met-induced gastrin release, suggesting that Met did not stimulate GRP release. Aromatic amino acids did not strongly influence gastrin release. Medium chain triacylglycerol, which is rapidly hydrolyzed to fatty acids in the lumen, strongly stimulated gastrin secretion but long chain triacylglycerol had no effect. The data suggest that amino acids (Met, Arg and His) and fatty acids, but not triacylglycerol, are gastrin releasing factors in birds while acid inhibits secretion: there are therefore both similarities and differences between birds and mammals in the control of gastrin release.
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PMID:The regulation of gastrin secretion in the chicken. 776 24

The aim of this study was to characterize the receptor(s) for bombesin (BN) and its homologues (gastrin releasing peptide, GRP; neuromedin B, NMB; neuromedin C, NMC) in guinea pig gallbladder muscle strips. Dose-dependent contractions were induced by all peptides tested (potency: BN = GRP > NMC > NMB, but with similar efficacy: BN = GRP = NMC = NMB). The contractions were resistant to tetrodotoxin, atropine, phentolamine, and propranolol. BN tachyphylaxis (1 microM) abolished subsequent contractile responses to BN, GRP and NMC; and partially antagonized the response to NMB (66 +/- 7% inhibition). NMB tachyphylaxis (10 microM) markedly inhibited subsequent contractile responses to NMB (78 +/- 5%); and partially antagonized the contractile response to BN (36 +/- 4%), GRP (31 +/- 12%) and NMC (22 +/- 2%). At 1 microM, both [D-Phe6, Des-Met14]-BN(6-14) ethylamide and ICI 216, 140, two BN receptor antagonists, reduced the contractile actions of BN (82 +/- 4% and 59 +/-8% inhibition, respectively), GRP (75 +/- 11% and 45 +/- 5%), and NMC (73 +/- 9% and 51 +/- 6%) while having no marked effect on NMB contractions. Our pharmacological approaches (receptor tachyphylaxis and differential antagonism) provide support for two types of receptors for BN-like peptides on guinea pig gallbladder smooth muscle: a GRP-preferring receptor and a NMB-preferring receptor.
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PMID:Pharmacological analysis of receptors for bombesin-related peptides on guinea pig gallbladder smooth muscle. 780 Aug 49


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