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

Guanylate cyclase in the guinea pig fundic mucosa occurred in two enzymatic forms: a "soluble" form and a particulate form. The mean basal activity of the soluble fraction measured in the presence of 300 micrometer guanosine-5'-triphosphate and 5 mM MnCl2 was 72.6 +/- 5.3 pmoles of cyclic GMP per mg of protein per min. Guanylate cyclase activity was dependent on Mn2+; it was increased by sodium azide (NaN3), CaCl2, cysteine, secretin, and cholecystokinin, but it was not influenced by gastrin, histamine, cholinergic esters, prostaglandins E1 and A1. NaN3 (1 mM) decreased the apparent Km for MnCl2 and potentiated the effects of MgCl2. The activity of the particulate fraction represented about 14% of that of the supernatant fraction. The guanylate cyclase activity of that fraction was not modified by NaN3, gastrin, cholinergic agents, secretin, or cholecystokinin. Cysteine inhibited its activity. These data do not support the hypothesis that cyclic GMP acts as a second messenger for the action of cholinergic agents and gastrin in the guinea pig gastric mucosa.
 ...
PMID:Effect of Ca2+, Mg2+, NaN3, cholinergic agents, and gastrointestinal hormones on the guanylate cyclase from guinea pig gastric mucosa. 2 35

The interrelationship of the effects of antacids and of rising intragastric pH on serum gastrin levels was examined by comparing the effect of three antacids (Mg(OH)2Al(OH)3, and CaCO3), and their nonbuffering chloride compounds (MgCl2, AlCl3, and CaCl2), on serum gastrin and intragastric pH in duodenal ulcer patients. In the case of calcium, the effect of CaCl2 with a pH of 10, and in another group, CaCl2 with a pH of 2, was studied. In the case of magnesium, a control group was also investigated. In another group, the effect of a nonionized suspension (BaSO4) was studied in order to assess the contribution of intragastric volume. Serum gastrin was determined radioimmunologically, and pH measurements were performed in vitro using a glass electrode. Serum gastrin concentrations rose significantly whenever intragastric pH was raised. Serum gastrin also rose after MgCl2, AlCl3, and CaCl2 with a pH of 2, when intragastric pH was not significantly altered. This rise, however, was significantly smaller than after administration of the antacids, except in the MgCl2-Mg(OH)2 and in the CaCl2 pH 10-CaCO3 groups. No significant rise of serum gastrin levels was observed after BaSO4. In nonulcer subjects, gastrin response was smaller than in the duodenal ulcer patients. The results suggest that administration of nonbuffering Mg-, Al-, and Ca-chlorides leads to elevated serum gastrin levels in duodenal ulcer patients; rising intragastric pH, however, exerts an additional serum gastrin response.
 ...
PMID:Effect of rising intragastric pH induced by several antacids on serum gastrin concentrations in duodenal ulcer patients and in a control group. 23

The experiments have been carried out on four intact awake dogs to study the influence of intragastric introduction of deionized water, 5 mmol/l of calcium and magnesium chloride solutions in a dose of 3 ml/kg on release of gastrin and insulin into blood. It is stated that during the first 4 min after infusion of deionized water the release of gastrin decreases by 89 +/- 32 conventional units (c.u.), CaCl2 exerts a more pronounced inhibitory effect (168 +/- 36 c.u.), while MgCl2, on the contrary, increases the gastrin release by 398 +/- 92 c.u. Atropin (0.03 mg/kg, subcutaneous injection, 10 min before infusion) absolutely takes away the gastrin-stimulating effect of magnesium, but it has almost no influence on the gastrin-inhibitory effect of calcium. The latter can be taken away by 62% by ornid (5 mg/kg subcutaneously, 20 min before infusion). Preliminary anaesthesia of the stomach mucosa by trymecain or novocain absolutely remove the effect of both calcium and magnesium. Insulin release remained significantly unchanged in any series of experiments.
 ...
PMID:[An analysis of the mechanism of the effect of intragastric calcium and magnesium on the release of gastrin and insulin in dogs]. 128 91

An organ culture system was utilized to examine the effect of gastrin (G-17-I) and epidermal growth factor (EGF) on colonic mucosal ornithine decarboxylase (ODC) activity, and the expression of the ODC gene. Exposure of colonic mucosal explants to either gastrin or EGF (50-500 ng/ml) for only 4 h resulted in a profound stimulation (150-600%) in ODC activity over the basal level. These increases were essentially abolished by difluoromethylornithine (DFMO; 2 nmol/ml) or CaCl2 (2 umol/ml). Gastrin also activated the ODC gene in the colonic mucosa as evidenced by increased steady-state ODC mRNA levels in the colonic mucosal explants after 4 h exposure to the hormone, when compared with the controls. It is concluded that colonic mucosal ODC is responsive to both gastrin and EGF.
 ...
PMID:Gastrin and epidermal growth factor induction of ornithine decarboxylase in rat colonic explants. 231 6

It has been hypothesized that secretin may act directly on gastrinoma through the adenylate cyclase system to cause stimulation of gastrin release. We studied gastrinoma cells in vitro to determine whether secretin would stimulate gastrin release directly and whether the gastrinoma cell membrane had a functional secretin receptor adenylate cyclase system. Fresh tumor was prepared in cell suspensions containing 1.5 X 10(6) viable cells and incubated for 2 hours with either 2 mM CaCl2 alone (control) or 2 mM CaCL2 and 0.025 U/ml secretin. The gastrin content of the cells in each incubation chamber and the medium were determined by radioimmunoassay and results were expressed as mean gastrin pg/microgram protein +/- SD. Under basal conditions the cellular gastrin content was 39.9 +/- 6.4 (control) compared with 16.7 +/- 2.1 (secretin). After 2 hours of incubation, cellular gastrin content increased in both groups: 68.5 +/- 11.9 (control) to 68.3 +/- 5.5 (secretin). However, the percent of gastrin released into the medium during incubation decreased by one half in both groups (control 37.3% +/- 4.0% to 22.2% +/- 3.0%; secretin 42.8% +/- 7.0% to 18.9% +/- 1.8%). Adenylate cyclase activity was assessed by measuring cAMP generation in fresh-frozen gastrinoma and cultured gastrinoma cell membranes. Isoproterenol (10(-5) M), PGE1 (10(-4) M), and GppNHp (guanine nucleotide) (10(-5) M) caused fivefold to 25-fold increases in cAMP generation. Secretin did not stimulate adenylate cyclase activity above basal (21.73 +/- 4.07 and 2.29 +/- 1.2 pmol cAMP/mg protein/min) for frozen and cultured gastrinoma, respectively. Secretin failed to stimulate gastrin release and adenylate cyclase in vitro. This suggests that secretin-stimulated gastrin release in vivo may not be due to a direct effect of secretin on the gastrinoma.
 ...
PMID:Failure of secretin to stimulate gastrin release and adenylate cyclase activity in gastrinoma in vitro. 609 76

The role of calcium in the stimulus-secretion coupling of antral gastrin release was examined in isolated sheets of canine antral mucosa. Mucosa was obtained from 137 dogs and mounted in Ussing chambers to separate the luminal from nutrient surfaces. The influence of verapamil, LaCl3, A23187, and EGTA on the release of gastrin by luminal calcium and ethyl alcohol was examined and the release of immunoreactive gastrin (IG) was measured in luminal perfusates. Release of IG by luminal calcium was dose-related, unsaturable, and impaired by verapamil and by LaCl3. Release of IG by alcohol was prevented by leaching the mucosa of calcium and restored by repletion of the calcium. IG release induced by alcohol was prevented by topical, but not by nutrient, application of LaCl3. Molecular sieve and affinity chromatography of the endogenous IG released in the absence of luminal calcium, and of the exogenous gastrin added, indicated that antral gastrin was released as heptadecapeptide gastrin, and that which was released in the presence of CaCl2 degraded rapidly into a C-terminal fragment. The data indicate that calcium may participate in the stimulus-secretion coupling of canine antral gastrin release in vitro.
 ...
PMID:Role of calcium in the stimulus-secretion coupling of antral gastrin release. 640 Dec 47

Two hundred millilitres of an isotonic solution of CaCl2 (0,118 M) were injected and left 15 min in the stomach of normal subjects (SN1; n = 21), of patients with gastric ulcer (UG; n = 16), patients with duodenal ulcer (UD; n = 40), patients with normochlorhydric gastritis (G1; n = 13) and patients with hypo- or achlorhydric gastritis (G2; n = 7). Gastric acid secretion and gastrinemia were measured during 90 min. After intragastric calcium injection, the acid secretion was increased during 60 min in almost all subjects (87 to 100 p. 100 of subjects in the various groups) whereas gastrin release was increased in the majority (57 to 84 p. 100) of cases. The possible dissociation between the acid and gastrinic responses implies that the calcium-induced acid response is independent of the calcium-induced gastrin release. During control experiments in normal individuals, continuous intragastric perfusion (300 ml/h) of NaCl 0.15 M failed to alter gastric acid secretion or gastrin release, whereas continuous intragastric perfusion of CaCl2 0,118 M enhanced gastric acid secretion and gastrin release. The action of CaCl2 0,118 M is therefore not attributable to gastric distension but directly to calcium itself. The stimulation of acid secretion by intragastric calcium was more conspicuous in patients with gastric or duodenal ulcer than in normal subjects. The release of gastrin was higher in gastritis and duodenal ulcer than in the normal group. It is hypothesized that intragastric calcium increases the cholinergic tone of the parietal cell.
 ...
PMID:[Effects of intragastric calcium on gastric acid secretion and release of gastrin in normal man and in various pathological cases]. 661 72

We studied effects of graded concentrations of intragastric calcium on acid secretion, residual gastric volume, and serum gastrin and calcium levels. Intragastric titration was performed with solutions of isotonic mannitol or mannitol plus 2.5, 6, 16, 39, and 97 mM CaCl(2) in 10 normal and eight duodenal ulcer subjects. Acid secretion was significantly increased above control values by the two highest CaCl2 concentrations in normal subjects and by the three highest CaCl2 concentrations in ulcer subjects. Highest observed acid output to any concentration of CaCl2 was 55% of peak acid output to pentagastrin in normal subjects and 75% in ulcer subjects. Intragastric calcium also released gastrin; correlation between acid secretion and circulating gastrin was weak (r = 0.43, P less than 0.05). Serum calcium was slightly increased but did not correlate with acid secretion. Residual intragastric volume after both control and CaCl2 solutions was much less in ulcer than in normal subjects; calcium did not alter residual volumes.
 ...
PMID:Effects of graded amounts of intragastric calcium on acid secretion, gastrin release, and gastric emptying in normal and duodenal ulcer subjects. 668 10

The hypocalcemic effect of gastrin and its possible mode of action were studied in rats. Gastrin (13 micrograms/100 g rat), injected intravenously led to a significant reduction in the plasma calcium concentrations. The release of endogenous gastrin by an intragastric phenylalanine instillation similarly led to a significant hypocalcemia in intact rat but not in antrectomized rat. Moreover, the protective role of endogenous gastrin against hypercalcemia induced by an intraduodenal infusion of CaCl2 (10 mg/100 g rat) was demonstrated. Gastrin (50 microgram/100 g rat) seems to have no influence on the net intestinal absorption of 45Ca. The removal of 45Ca from plasma was also unaffected by gastrin administration. The disappearance rate from plasma of 45Ca administered 17 hr previously was compared in sham, thyroidectomized (TX) and parathyroid-autotransplanted rats receiving saline or gastrin. The faster rate of disappearance of plasma 45Ca from plasma in gastrin-treated TX autoparathyroid-transplanted rats indicated the suppressive action of gastrin on the release of 45Ca from as yet unknown source(s).
 ...
PMID:Possible role and mode of action of gastrin on calcium homeostasis in the rat. 732 69

The ECL cells are histamine- and pancreastatin-secreting endocrine cells in the oxyntic mucosa, thought to release a blood Ca2+-lowering peptide hormone upon stimulation by gastrin. Previously, we have shown that the ECL cells do not respond to perturbations in blood Ca2+. In the present study, we examine if Ca2+ in the gastric lumen will affect the activity of the gastrin-ECL-cell axis. Freely fed or food deprived (48 h) rats were given an oral load of CaCl2 (or NaCl), and the blood Ca2+ concentration was monitored. The serum gastrin concentration at sacrifice, 3 h after ingestion of CaCl2, was measured together with two parameters of ECL cell activity: the oxyntic mucosal histidine decarboxylase (HDC) activity and the serum pancreastatin concentration. The circulating concentrations of calcitonin and parathyroid hormone (PTH) were also measured. Oral CaCl2 raised the blood Ca2+ in a dose-dependent manner. The two highest doses (which caused damage to the oxyntic mucosa) raised the serum gastrin concentration and the HDC activity in both fed and fasted rats; the serum pancreastatin concentration remained unaffected. Oral CaCl2 raised the serum calcitonin concentration and lowered the serum PTH concentration. The effects of high doses of oral CaCl2 on the serum gastrin concentration and on the oxyntic mucosal HDC activity could be reproduced by a high dose of NaCl. Thus the effects are probably not due to Ca2+ per se. We conclude that the gastrin-ECL-cell axis in the rat does not respond to peroral Ca2+. Since the ECL cells do not respond to either circulating or peroral Ca2+ they are unlikely to secrete a calciotropic hormone.
 ...
PMID:Evidence that peroral calcium does not activate the gastrin-ECL-cell axis in the rat. 955 80


1 2 Next >>