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)

The basal and gastrin-stimulated gastric acid output was measured in rats with a distal splenocaval shunt. In addition, serum gastrin levels were determined in rats with splenocaval and portacaval shunts. The rise in gastric acid output with increasing gastrin dosage was the same in rats with splenocaval shunt as in the controls. Serum gastrin levels were not influenced by portocaval or splenocaval shunting.
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PMID:[Gastric secretion and gastrin values following portocaval and splenocaval shunts in the rat]. 2 62

Gastric secretion and fasting plasma gastrin levels were investigated in 26 patients with bilharzial hepatic fibrosis and 26 controls. The groups did not differ in their basal secretion. When stimulated by intravenous infusion of histamine the maximal acid output in patients with bilharzial hepatic fibrosis was significantly less than in the control group. This was unlikely to be a result of neutralisation by reflux of alkaline duodenal contents as the volumes of reflux were not different from control subjects, but was compatible with a true reduction in gastric secretion as assessed by two-component hypothesis. Neither the lowered gastric acidity nor the liver damage in patients with bilharzial hepatic fibrosis correlated with circulating gastrin. The fasting levels of plasma gastrin in these patients were not different from controls. As in other liver diseases the cause of diminished gastric secretion remains unclear.
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PMID:Gastric secretion and basal gastrin concentration in bilharzial hepatic fibrosis. 3 Jun 81

Gastric acid secretion stimulated by a normally eaten beefsteak meal was measured for 4 h in 16 patients with duodenal ulcer disease (DU), in 9 patients with gastric ulcer disease (GU), and in 14 controls by intragastric titration with bicarbonate to a constant pH 5.5. Reproducibility of the method investigated in 6 DU and in 5 controls gave similar acid secretory values (var. coeff. = 7.5%). DU produced acid on a higher level and with longer duration after food than controls and GU (p less than 0.001). Apart from the second half of the first hour after food, when the acid secretion was higher in controls than in GU (p less than 0.025), there was no significant difference in acid output after food between GU and controls. Maximum gastrin values and 'total gastrin output' after food were significantly higher in GU than in controls, but these differences were not significant between GU and DU and between DU and controls. Fasting gastrin and gastrin levels after food were not correlated to basal acid output or acid output after pentagastrin or food in any of the groups. The maximal acid output after food was higher than the peak acid output after pentagastrin in controls, DU and GU. The relation between food- and pentagastrin-stimulated acid output was not statistically significantly different between the three groups. Instead, acid secretion after food was well correlated to acid secretion after pentagastrin in controls, DU and GU (r = 0.85).
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PMID:Food-stimulated acid secretion measured by intragastric titration with bicarbonate in patients with duodenal and gastric ulcer disease and in controls. 3 74

A conventional pentagastrin test was carried out in 25 patients with dyspeptic complaints, and gastric H+ and pepsin outputs were determined. Blood was drawn before the intubation and 5 and 30 min after subcutaneous injection of pentagastrin, and serum group I pepsinogens (PG I) and serum gastrin were determined by radioimmunoassay methods. A significant correlation was found between serum PG I, on the one hand, and basal gastric pepsin, output as well as pentagastrin-stimulated gastric H+ and pepsin outputs, on the other. Basal serum gastrin was also significantly correlated to pentagastrin-stimulated gastric pepsin output as well as to serum PG I. Pentagastrin failed to induce an increase in serum PG I during the first 30 min.
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PMID:Serum group I pepsinogens and gastrin in relation to gastric H+ and pepsin outputs before and after subcutaneous injection of pentagastrin. 3 75

In acute experiments on cats antral pouches were perfused with solutions of different pH (1-13). After antrum passage the gastrin levels in the perfusates were measured with radioimmunoassay and the amounts of gastrin released into the antral lumen per minute calculated. The venous gastrin levels were determined concomitantly. Small amounts of gastrin (1,000--1,500 pg/min) were released into the antrum during perfusion with 0.1 M HCl. Subsequent perfusion with 0.15 M NaCl (pH 6.8) did not significantly increase the release of gastrin. On the other hand, 0.1 M phosphate buffer (pH 7.4) caused a dramatic augmentation of the gastrin output into the antral lumen (approximately 17 fold). A concomitant increase of peripheral gastrin levels was observed. Also other alkaline solutions such as 0.15 M NaHCO3 (pH 8), 0.15 M Tris buffer (pH) or 0.01 and 0.1 M NaOH (pH 12 and 13) promoted the release of gastrin. It is discussed whether the gastrin release at alkaline pH is induced by the alkaline pH itself or by anions such as HPO-4, HCO-3 and OH-. The apparent effect of pH could then be due to the formation of these ions at higher pH.
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PMID:Effect of intraantral pH on basal gastrin release into the circulation and antral lumen in anesthetized cats. 3 63

Biochemical assays on microdissected samples, denervation studies, subcellular fractionation, and light and electron microscopic autoradiography of high affinity uptake have been performed to study the cellular localization of transmitter candidates in the rat hippocampal formation. High affinity uptake of glutamate and aspartate is localized in the terminals of several excitatory systems, such as the entorhino-dentate fibres (perforant path), mossy fibres (from granular cells) and pyramidal cell axons. Thus, in stratum radiatum and oriens of CA1, 85% of glutamate and asparate uptake and 40% of glutamate and aspartate content are lost after lesions of ipsilateral plus commissural fibres from CA3/CA4. Hippocampal efferents also take up aspartate and glutamate, since these activities are heavily reduced in the lateral septum and mamillary bodies after transection of fimbria and the dorsal fornix. The synthesis (by glutamic acid decarboxylase), content and high affinity uptake of gamma-aminobutyrate (GABA) are not reduced after lesions of these or other projection fibre systems. A localization in intrinsic neurons is confirmed by a selective loss of glutamic acid decarboxylase after local injections of kainic acid. Peak concentrations of the enzyme occur near the pyramidal and granular cell bodies, corresponding to the site of the inhibitory basket cell terminals, and in the outer parts of the molecular layers. Some 85% of glutamic acid decarboxylase is situated in 'nerve ending particles'. Acetylcholine synthesis (by choline acetyltransferase) disappears after lesions of septo-hippocampal fibres. Since 80% of the hippocampal choline acetyltransferase is in 'nerve ending particles', the characteristic topographical distribution of this enzyme should reflect the distribution of cholinergic septo-hippocampal afferents. Serotonin, noradrenaline, dopamine and histamine are located/synthesized in afferent fibre systems. Some monoamine-containing afferents to the hippocampal formation pass via the septal area, others via the amygdala. The hippocampal formation also contains nerve elements reacting with antibodies against neuroactive peptides, such as enkephalin, substance P, somatostatin and gastrin/cholecystokinin.
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PMID:Localization of putative transmitters in the hippocampal formation: with a note on the connections to septum and hypothalamus. 3 19

The serum levels of immunoreactive gastrin (IRG) and secretion of gastric juice were simultaneously determined in dogs anesthetized with morphine and urethane. There was a significant positive linear correlation between secretion and serum IRG level in these dogs. Serum IRG level and gastric secretion were reduced by bilateral vagotomy at the neck. The amount of gastric juice was reduced dose-dependently by an intravenous injection of atropine (0.001--0.016 mg/kg), hexamethonium (0.064--1 mg/kg) and secretin (2--8 U/kg). The reduction of gastric secretion paralleled that of the serum IRG level. However, the reduction of gastric secretion did not parallel that of serum IRG level under the influence of prostaglandin E1 (0.002--0.008 mg/kg i.v.) and duodenal acidification. Prostaglandin E1 and duodenal acidification reduced gastric secretion without the reducing serum IRG level. These findings were discussed in relation to the mechanism of gastric juice stimulation by morphine, and it is suggested that endogenous gastrin release through the vagal and non-vagal pathways participates in morphine-induced gastric secretion. The difference in inhibitory effect between duodenal acidification and secretin suggests the possibility that substances other than secretin may participate in the regulation of gastric secretion in dogs.
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PMID:Relationship between gastric secretion and serum gastrin levels in dogs anesthetized with morphine and urethane. 3 15

The effect of some tripeptides, which are fragments of peptide hormones, and their analogs on the content of biogenic monoamines (BM) from albino mice brain was studied. It was found that thyroliberin, melanostatin and the C-terminal tripeptide of gonadoliberin activate the dophaminergic (DA-ergic) system in the forebrain of mice treated with reserpine or haloperidol, whereas the C-terminal tripeptide of gastrin acts as a synergic blocker of the DA receptors. The N-terminal tripeptides (with and without the amido group) do not affect the content of BM. No effect of the tripeptides was observed in intact animals. It is assumed that the agonistic or antagonistic effect of the tripeptides on BM is due to certain structural peculiarities of the tripeptides, e.g. the presence of the C-terminal amido group and their endogenous nature.
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PMID:[Effect of some fragments of peptide hormones on the content of biogenic monoamines from mouse brain]. 3 28

Mean fasting levels of pancreatic polypeptide (PP) in 24 patients with Zollinger-Ellison syndrome (ZES) and in 12 patients with hyperparathyroidism originating from families with multiple endocrine adenomatosis type I (MEAI-HPT) were significantly higher than in 72 normal controls. The overlap between the 3 groups, however, was large. In patients with ZES, increased PP levels were not related to the presence of MEAI or metastases; nor was there a correlation between serum PP and gastrin concentrations. The post-prandial PP release in 10 ZES patients and in 10 patients with MEAI-HPT was lower than in 9 normal controls. The physiological significance of the present findings is unclear.
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PMID:Serum levels of pancreatic polypeptide in Zollinger-Ellison syndrome, and hyperparthyroidism from families with multiple endocrine adenomatosis type I. 3 34

A pressure and pH-sensitive probe has been constructed for simultaneous measurement of gastro-oesophageal sphincter pressure and intragastric pH. The coefficient of variation for measurements of the gastro-oesophageal sphincter was 0.24, and for the intragastric pH, 0.09. After peroral ingestion of 400 mg of cimetidine or placebo, simultaneous measurements of gastro-oesophageal sphincter pressure and intragastric pH were made at fixed time intervals, and at the same time blood samples were taken for determination of serum gastrin and serum cimetidine concentrations. No demonstrable difference was found in the time-course of the gastro-oesophageal sphincter pressure after ingestion of cimetidine or placebo. After ingestion of cimetidine a significant rise in intragastric pH (p less than 0.05) occurred after 40 min, and this increased pH was maintained for the remainder of the experimental period, corresponding to a serum cimetidine concentration of over 1.00 mg/l. Similarly, there was a significant rise (p less than 0.05) in serum gastrin concentration after 150 min. There was a significant direct correlation between corresponding measurements of intragastric pH and serum gastrin (p less than 0.001), between intragastric pH and serum cimetidine (p less than 0.001), and between serum gastrin and serum cimetidine (p less than 0.05). Ingestion of cimetidine results in an increase in the serum gastrin concentration in healthy subjects, presumably as a result of reduced secretion of acid in the stomach. Neither the endogenous increase in serum gastrin concentration nor the increase in intragastric pH causes alteration in the gastro-oesophageal sphincter pressure.
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PMID:The influence of cimetidine on basal gastro-oesophageal sphincter pressure, intargastric pH, and serum gastrin concentration in normal subjects. 3 25


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