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)

1. Secretagogues of pancreatic enzyme secretion: pancreozymin, carbamylcholine, gastrin I, the octapeptide of pancreozymin, caerulein and the Ca2+ ionophore A 23187 stimulate 45Ca uptake into isolated rat pancreatic cells, whereas adrenaline, isoproterenol, secretin, dibutyrylic cyclic adenosine 3',5'-monophosphate and dibutyrylic cyclic guanosine 3',5'-monophosphate have no effect on 45Ca uptake. 2. A graphical analysis of the Ca2+ uptake curves reveals at least two phases: a fast phase, probably due to binding of Ca2+ to the membrane and a slow phase representing Ca2+ transport into cells. Both phases are stimulated by pancreozymin and carbamylcholine. 3. The 45Ca-exchangeable pool size is increased by both carbamylcholine and pancreozymin, whereas a significant increase of total content of cell calcium was too small to be detected. 4. Atropine blocks the stimulatory effect of carbamylcholine completely but not that of pancreozymin. The Ca2+ antagonist D600 blocks the stimulatory effects of both carbamylcholine and pancreozymin only partially. 5. The data suggest that secretagogues of pancreatic enzyme secretion act by increasing the rate of Ca2+ transfer into the cell most probably through an increase of the cell membrane permeability for Ca2+.
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PMID:Calcium ion uptake in isolated pancreas cells induced by secretagogues. 17 97

Vagal activation produces a gastric acid secretory response by direct nervous stimulation of the parietal cell area and, at least in dogs, by gastrin released mainly from the antrum. In duodenal ulcer (DU) patients antrectomy reduces the acid response to sham feeding slightly more than the maximal acid output in response to pentagastrin, indicating that an antral factor contributes to the acid secretion induced by sham feeding. The marked acid response to sham feeding in antrectomized patients suggests that the direct nervous stimulation of the acid-secreting glands is the predominating stimulus in the vagal activation of acid secretion in man. In the present study vagal activation has been induced by adequate and modified sham feeding and insulin hypoglycemia in DU patients and healthy subjects. The acid response to adequate and modified sham feeding amounted to about 50% of the peak acid output in response to pentagastrin and corresponded to the acid response to an insulin dose of 0.1 U/kg b.w. Modified sham feeding seems to be a simple method of inducing physiological vagal activation of acid secretion. Sham feeding for 15 min increased only insignificantly the plasma concentrations of total gastrin immunoreactivity or heptadecapeptide gastrin. Prolonged sham feeding during intragastric neutralization or sham feeding after proximal gastric vagotomy did not significantly increase the plasma gastrin concentrations. Sham feeding is obviously a poor stimulus for release of gastrin in man. Either release effect of very small amounts of gastrin-17 or release of non-established gastrins may explain the biological effect of an antral factor. Pretreatment with benzilonium, an anticholinergic drug with minimal cerebral actions, increased the gastrin concentration after sham feeding in about half the experiments. This heterogeneous effect supports a non-cholinergic vagal release of gastrin and a cholinergic inhibition of gastrin release but also indicates a complex interaction at the level of the gastrin cells during vagal activation. Evidence for an inhibitory vagogastrone mechanism in DU patients has been found but its effect is weak and transient. Proximal gastric vagotomy abolished the acid responses to both insulin hypoglycemia and sham feeding, in accordance with the view that the direct nervous excitation of the acid-secreting glands is the predominating stimulus in the vagal activation of gastric acid secretion in man. Atropine in low doses or benzilonium inhibited the acid response to sham feeding by only 65%. This finding suggests that the direct vagal excitation of the acid-secreting glands is mediated only partially by cholinergic neurotransmission. Gastric acidification inhibited the gastric acid secretory response to insulin hypoglycemia both in healthy subjects and in DU patients. The inhibitory effect was significantly less in DU patients, however, supporting the concept of a defective inhibition by antral acidification in DU patients.
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PMID:Studies on vagal activation of gastric acid secretion in man. 29 Dec 98

Cimetidine markedly inhibits gastric acid secretion, but from the therapeutic point of view it is important to know whether concurrent treatment with an anticholinergic increases its effect. This possibility has been investigated by measuring the 24 h intragastric acidity and nocturnal output of acid in four duodenal ulcer patients, each receiving on separate occasions cimetidine 1 g/day and placebo, atropine 2-4 mg/day and placebo, cimetidine and atropine, or two placebos. Cimetidine alone decreased mean hourly hydrogen ion activity by 63% of control values, decreased mean hourly hydrogen ion concentration (total acid) by 41%, inhibited nocturnal acid secretion by 83% and resulted in half the nocturnal samples being anacidic. Atropine alone had no effect when compared with control and combined treatment with both drugs was not superior to cimetidine alone. Atropine did not affect the absorption or urinary excretion of cimetidine. Fasting serum gastrin concentrations were not changed by any of the treatments. At the doses studied, the combination of cimetidine with an anticholinergic appears to offer no advantages over treatment with the H2-antagonist alone. Cimetidine is the only potent anti-secretory drug that does not cause acute side-effects and this important advantage would be lost if it were given with a maximal dose of an anticholinergic.
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PMID:24-hour intragastric acidity and nocturnal acid secretion in patients with duodenal ulcer during oral administration of cimetidine and atropine. 32 18

In 10 healthy subjects and 25 duodenal ulcer patients, gastric acid and pepsin and serum gastrin responses to cephalic-vagal stimulation induced by modified sham-feeding (MSF) were studied before and after vagotomy and atropinisation and compared with those to maximal stimulation with pentagastrin. When the MSF-induced peak acid output was normalised as a percentage of peak response to pentagastrin it was about 62% in healthy subjects and 66% in duodenal ulcer patients. Serum gastrin concentration was not changed significantly by modified sham-feeding either in normal subjects or in duodenal ulcer patients. Truncal vagotomy completely abolished gastric acid and pepsin responses to MSF in duodenal ulcer patients. Atropine almost completely suppressed gastric acid and pepsin responses to MSF in healthy subjects and reduced those in duodenal ulcer patients by about 62%. The combination of the modified sham-feeding and pentagastrin infusion resulted in augmentation of the acid output in duodenal ulcer patients but not in healthy subjects. This study shows that the cephalic phase results in a potent gastric acid and pepsin stimulation which is not accompanied by any change in serum gastrin concentration either in healthy subjects or duodenal ulcer patients and which is abolished by vagotomy and suppressed by atropine.
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PMID:Cephalic phase of gastric secretion in healthy subjects and duodenal ulcer patients: role of vagal innervation. 39 56

Plasma gastrin concentrations and gastric acid output after modified sham feeding were determined in 20 duodenal ulcer patients. Sham feeding produced an acid response corresponding to 40-68% of the maximal acid output after pentagastrin stimulation, with no significant increase of plasma gastrin concentrations. In eight patients proximal gastric vagotomy almost abolished the acid responses to both insulin hypoglycaemia and sham feeding. Sham feeding in the vagotomised patients did not change the gastrin concentrations in plasma. After pretreatment with benzilonium, an anticholinergic with minimal central nervous effects, plasma gastrin concentrations increased after sham feeding. The study confirms that sham feeding is a poor stimulus for gastrin release in duodenal ulcer patients and supports a cholinergic inhibition of gastrin release. Intravenous injection of benzilonium bromide in a dose close to 70 micrograms/kg, and atropine in the low dose of 30 micrograms/kg inhibited the acid response to sham feeding by about 65%. Atropine in a dose of 50 micrograms/kg virtually abolished the acid sham feeding response, possibly owing to ganglionic or central nervous blockade. Vagal activation of the acid secretory glands does not seem to involve a purely cholinergic neurotransmission.
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PMID:Effect of proximal gastric vagotomy and anticholinergics on the acid and gastrin responses to sham feeding in duodenal ulcer patients. 39 71

To study the relation between gastrin released by vagal excitation and the secretion of H+ and pepsin under various conditions, central vagal excitation was induced by 2-deoxyglucose (2DG) in doses of 50, 100, and 200 mg/kg body wt given as a single intravenous injection in seven gastric fistula dogs, three with fundic vagotomy and four with intact vagi. Serum gastrin increased linearly with dose doubling in both groups but was twice as high in the vagotomized dogs. Total acid output for 3 h was related linearly to integrated gastrin output in both groups, but the slope, H+/gastrin, was 10 times steeper in the vagally intact dogs (330 vs. 34 mueq/pg gastrin-ml-30 min) and pepsin output almost 20 times greater [5,400 peptic units (PU) vs. 296 PU]. Acidification of the antrum to pH 1.2-1.4 eliminated the gastrin response to 2DG in both groups of dogs. Atropine (100 microgram/kg iv) reduced serum gastrin in the vagotomized and increased it in the intact dogs. Atropinization uncovers stimulation by 2DG by pathways that do not involve muscarinic cholinergic receptors. Stimulation by both pathways is suppressible by acid. We conclude that fundic vagotomy removes an inhibitor of vagal gastrin release.
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PMID:Augmented vagal release of antral gastrin by 2-deoxyglucose after fundic vagotomy in dogs. 42 Feb 87

We studied the effect of several doses of atropine on the serum gastrin and pancreatic polypeptide responses to vagal stimulation in healthy human subjects. Vagal stimulation was induced by sham feeding. To eliminate the effect of gastric acidity on gastrin release, gastric pH was held constant (pH 5) and acid secretion was measured by intragastric titration. Although a small dose of atropine (2.3 mug/kg) significantly inhibited the acid secretory response and completely abolished the pancreatic polypeptide response to sham feeding, this dose of atropine significantly enhanced the gastrin response. Higher atropine doses (7.0 and 21.0 mug/kg) had effects on gastrin and pancreatic polypeptide release which were similar to the 2.3-mug/kg dose. Atropine (0.78 and 2.3 mug/kg) without sham feeding significantly inhibited basal acid secretion and also led to significant increases in serum gastrin above basal levels. The gastrin response to sham feeding with 2.3 mug/kg atropine was significantly greater than the sum of the gastrin responses to sham feeding alone and to 2.3 mug/kg atropine alone, indicating potentiation of vagal gastrin release by atropine. We conclude: (a) Unlike vagally mediated gastric acid secretion and pancreatic polypeptide release which can be blocked by atropine, vagal gastrin release is potentiated by atropine. This observation suggests the existence of a vagal-cholinergic pathway which normally (i.e., in the absence of atropine) inhibits gastrin release. (b) Because atropine (without sham feeding) increased basal gastrin levels, it is likely that the cholinergic pathway which inhibits gastrin release is active even when the vagus nerve is not stimulated by sham feeding.
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PMID:Effect of atropine on vagal release of gastrin and pancreatic polypeptide. 42 55

Effect of intravenously administered bombesin has been studied on the in vivo and in vitro motor function of the lower esophageal sphincter (LES) of the opossum. Intraesophageal pressures were monitored by an assembly of polyvinyl catheters attached to pressure transducers and a recorder. The catheters were continuously perfused with bubble-free water. Intravenous administration of 5, 10, 30, 50, and 100 ng/kg bombesin stimulated the LES 4, 34, 106, 148, and 130%, respectively, above control values. Atropine and hexamethonium did not antagonize the response of the LES to bombesin. Tetrodotoxin, phentolamine, and reserpine all significantly antagonized the response of the LES to bombesin. The LES stimulatory effect of bombesin injected locally in the left gastric artery (LGA) was antagonized significantly by local administration of phentolamine in the LGA. Experiments performed in vitro (25 ml baths containing oxygenated Krebs solution) showed that bombesin (10(-9) M) increased the tone of LES strips, and the effect was antagonized by phentolamine (10(-6) M). Serum gastrin concentrations increased significantly only 15 min after bombesin administration. It is concluded that bombesin is a potent stimulant of the LES. The mechanism of stimulation involves a direct effect on the smooth muscle as well as an indirect one by an effect on the postganglionic adrenergic neurons releasing norepinephrine.
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PMID:Mechanism of lower esophageal sphincter stimulation by bombesin in the opossum. 43 39

The ingestion of 2 different water loads (7.5 and 15 ml/kg) by healthy subjects stimulated the release of plasma motilin, gastrin, pancreatic polypeptide and VIP. Atropine was found to block the release of PP but not the other hormones.
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PMID:Release of gastrointestinal hormones following an oral water load. 51 May 7

Intracellular microelectrode technique and standard organ bath technique were used to investigate the effects of pentagastrin, G17, and G34 on the electrical and mechanical activities of canine antral circular muscle. All three molecular forms increased the amplitude and duration of the plateau of the gastric action potential and the frequency of spontaneous action potentials. They also increased the amplitude and frequency of spontaneous contractions. G17 was equal to or less potent than pentagastrin in all of its actions on this tissue. G34 had an equal or greater activity than G17. The electrical studies indicate that G17 is active in this tissue in a physiological range of concentrations. The ED50 for the effect of G17 to increase the amplitude of the plateau potential is less than that for the effect of G17 on gastric secretion, indicating that this is a physiological action of gastrin. Atropine studies indicate that only part of the in vitro inotropic action of gastrin is caused by the release of acetylcholine from nerve terminals, but that the chronotropic action is attributable to a direct effect on the smooth muscle membrane.
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PMID:Effects of pentagastrin, G17, and G34 on the electrical and mechanical activities of canine antral smooth muscle. 68 Apr 95


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