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)

Four cases of Barrett's esophagus are presented. Three cases presented with significant esophageal bleeding and one case presented with high esophageal stricture. Gastrointestinal panendoscopy was done in each case and multiple biopsies were taken. The biopsies were utilized for histomorphology, pepsinogen agar gel electrophoresis, and tissue gastrin assays. Tissue gastrin levels in esophageal mucosa were elevated in 2 cases when compared to controls with and without hiatus hernia. Pepsin and acid secretory studies were done by isolating the esophagus. Barrett's esophagus was shown to produce pepsin by both chemical studies (2 cases) and agar gel electrophoresis at pH 5.7 (3 cases), and was also shown to produce acid. The mucosa contained either cathepsin or cathepsin and pepsinogens in all cases. Nissen's fundoplication was performed in all of the patients. Of 3 patients who were bleeding, 2 who consented for this operation stopped bleeding after the operation. It is to be noted that the usual clinical treatment of antacids, bedrest, and raising the head end of the bed failed in all of the patients. The follow-up of 9 months to 3 years postoperatively has shown persistence of Barrett's mucosa with no evidence for any reversion to normal esophageal type.
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PMID:Pepsin secretion, pepsinogen, and gastrin in "Barrett's esophagus." Clinical and morphological characteristics. 77 Feb 25

In 32 healthy male volunteers the effects on gastric secretion of three methyl analogues of prostaglandin (PG) E2 have been studied, namel, 15 (R) -15-methyl PGE2 methyl ester, 15 (S) -15-methyl PGE2 methyl ester, and 16, 16-dimethyl PGE2. Secretion was measured for 30 min and a PG analogue at doses ranging from 1.25 to 2.5 mug per kg or a placebo was administered. Gastric secretion was then stimulated either by an intravenous infusion of pentagastrin (2 mug per kg-hr) or by a peptone meal with acid secretion determined by intragastric titration technique. The tests were randomized and double blind. All three methyl PG analogues exhibited a profound and prolonged inhibitory action on gastric acid and pepsin secretion induced by pentagastrin. PG analogues caused almost complete inhibition of gastric acid response to a peptone meal accompanied by a significant reduction in the serum concentration of immunoassayable gastrin. Except with the highest dose of PG (S) -15-methyl PGE2 methyl ester, which caused abdominal discomfort and single episodes of diarrhea in some subjects, no symptoms or untoward biochemical effects were observed. It is concluded that these methylated PG analogues are very potent inhibitors of gastric acid and pepsin secretion stimulated by pentagastrin or a meal and may have clinical potential in the treatment of peptic ulcer.
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PMID:Comparison of methylated prostaglandin E2 analogues given orally in the inhibition of gastric responses to pentagastrin and peptone meal in man. 77 Feb 26

Isoproterenol infusions depress pentagastrin (PG)-stimulated secretion of acid and pepsin from both gastric fistulae and denervated (Heidenhain) pouches in conscious dogs. It was not found to do so if methacholine replaced gastrin. Propranolol reversed the isoproterenol depression of PG stimulation but had no effect on isoproterenol plus methacholine except on the fistula where both acid and pepsin were depressed. It is felt that PG and methacholine act by differing mechanisms both on chief and parietal cells.
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PMID:Adrenergic activity and gastric secretion. 77 88

In 14 healthy male volunteers the effect of 16,16-dimethyl PGE2 methyl ester (PG/D) on gastric secretion have been studied. Gastric secretion was stimulated by an intravenous infusion of pentagastrin (2 mug/kg/h) with gastric juice collected by aspiration or by a pepton meal with acid secretion determined by intragastric titration technique. Intragastrical administration of PG(D) resulted in a strong decrease of gastric acid and pepsin secretion in tests with pentagastrin. PG(D) caused almost complete inhibition of gastric acid response to a pepton meal accompanied by a marked decline of pepsin concentration in the gastric juice as well as significant reduction in the serum level of immunoassayable gastrin. No side effects were noted during or in succeeding 24 hours after administration of PG(D).
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PMID:Effect of 16, 16-dimethyl prostaglandin E2 methyl ester on gastric secretion induced by pentagastrin and pepton meal in man. 77 88

In 6 healthy students, the gastric secretion of acid, pepsin, and IF was measured during one hour at basal conditions, and during one hour of stimulation with 0.01 mug/kg/h and thereafter during one hour of stimulation with 0.1 mug/kg/h of pentagastrin. On separate days the same dose of pentagastrin was given in combination with 0.15 mug/kg/h or 1.5 mug/kg/h of carbachol, or stimulation was performed with each of the two doses of carbachol alone. A dose-dependent relationship was found between carbachol and the output of acid, pepsin, and IF. The responses to carbachol were independent of changes in plasma gastrin concentration. The acid- and IF-secretions stimulated by the largest dose of pentagastrin were significantly increased by the largest dose of carbachol, whereas the secretion of pepsin was not. Pentagastrin and carbachol seem to interact by competitive augmentation on the gastric secretion of acid and IF.
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PMID:Gastric secretory response to different doses of carbachol and pentagastrin in man. 77 4

1. The peptic responses to Boots, GIH and synthetic secretins have been compared in fasting anaesthetized cats in which the pylorus and bile duct were occluded to prevent the release of duodenal hormones by acid and bile salts. A quantity of dilute acid introduced into the stomach at regular intervals ensured the total recovery of viscid secretions and preserved peptic activity. 2. The mean peak outputs of pepsin obtained in response to Boots secretin were significantly greater than the mean peak outputs of pepsin stimulated by equipotent doses of GIH secretin (4 Crick-Harper-Raper units of Boots secretin have been shown to stimulate a flow of juice and bicarbonate from the pancreas equal to that produced by 1 clinical unit of GIH secretin). The maximum output of pepsin stimulated by Boots secretin, 16 C.H.R. u./kg hr was 3 times the observed maximum output in response to the 4 times more potent dose of GIH secretin, 16 c.u./kg hr. The slopes of the log dose-response lines were significantly different for these two products indicating that their modes of action in stimulating pepsin may not be identical. 3. The outputs of pepsin following GIH and synthetic secretin were similar. Both these secretins stimulated the secretion of pepsin when infused in doses which stimulated the pancreas supramaximally. The less pure product Boots secretin evoked significantly higher peptic responses at doses submaximal for pancreatic stimulation, suggesting that a substance other than secretin exists in Boots preparations which contributes significantly to the overall output of pepsin in response to this product. The peptic response which was accompanied by a slight increase in acid output, but without any increase in pancreatic lipolytic activity, was not inhibited by atropine. This substance which is not present in highly purified GIH secretin does not appear to be cholic acid, gastrin, pancreozymin, glucagon or insulin. 4. The possibility that a vasodilator substance is present in Boots secretin which by expanding the splanchnic bed increases the concentration of secretin at target sites in the stomach and pancreas seems unlikely, as the flow of pancreatic juice does not increase proportionately with the vast increase in pepsin. A vasodilator substance which specifically affects the gastric vasculature remains a theoretical but unlikely explanation for our observation.
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PMID:A comparison of the pepsin stimulating effects of secretin preparations. 78 Dec 17

The effect os somatostatin (0.6 mg/hour) on insulin-stimulated gastrin release and gastric secretion of acid, pepsin, and IF has been examined in 6 unoperated patients with duodenal ulcer. Gastrin release and gastric secretion of acid, pepsin, and IF in response to insulin alone (0.15 IU/kg bw. iv.) were significantly reduced by simultaneous administration of somatostatin. This finding indicates an inhibitory effect of somatostatin on insulin-induced gastrin release and gastrin secretion in addition to the already known effects of somatostatin.
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PMID:Somatostatin inhibits insulin-stimulated gastrin release and gastric secretion of acid, pepsin, and intrinsic factor (IF) in duodenal ulcer patients. 78 89

Motilin is a polypeptide containing 22 amino-acids from the entero-chromaffin cells of the mucosa of the small intestine. Synthetic analogues (13-norleucine-motilin; 13-leucine-motilin) proved to be equal to the natural polypeptide in the biological aspects. Motilin primarily stimulates the motility of the upper gastrointestinal tract but inhibits gastrin evacuation. The contractile action of motilin does not take place by way of the nerves but through receptors on or in the smooth muscle cell itself. Motilin and cyclic adenosine-3':5'-monophosphate are functional antagonists in the contraction of the gastrointestinal musculature. Depending on the dosis, motilin increases gastric pepsin secretion and inhibits protein biosynthesis in the gastric mucosa itself. Radioimmunological motilin tests will help to determine which of the above-mentioned motilin actions are "physiological" and which of them merely "pharmacological".
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PMID:[Motilin-range and analysis of its action]. 78 38

The role of the sympathetic nerve supply to the gastric mucosa in gastric physiology is discussed. It is concluded that they are inhibitory to gastric acid secretion, mucosal blood flow, pepsin secretion, gastric oxygen consumption and that these nerves also decrease the serum gastrin concentration. Sympathetic nerve stimulation always reduces the mucosal blood flow and it is suggested therefore, that the inhibition of gastric secretion could be secondary to vasoconstriction mediated by noradrenaline release. The evidence for these conclusions is considered alongside the available histological evidence. It is concluded that the remaining hurdle is to place these phenomena within our knowledge of gastric physiology.
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PMID:A review: the agents and actions of sympathetic nerve and catecholamine inhibition of gastric mucosal function. 78 79

1. Experiments were performed on chloralose anaesthetized cats and gastric mucosal blood flow, acid and pepsin secretions were measured. Gastric mucosal pepsin and protein contents were measured at the end of the experiments which were done in three groups: gastrin (A), vagal (B), vagal and sympathetic nerve (C) stimulations. 2. Vagal stimulation significantly reduced (76%) the pepsin content of gastric mucosa compared with gastrin stimulated animals, none of which secreted pepsin. 3. The sum of the secreted and extracted pepsins for all the three groups was not significantly different. There was no significant difference in the extracted protein from any of the groups. 4. Gastric mucosal blood flow, acid and pepsin outputs all had significant correlations with time during the first 70 min of vagal stimulation. During the period 80-160 min of vagal stimulation acid secretion and mucosal blood flow were not correlated with time but pepsin output declined significantly. From 170 to 220 min of vagal stimulation, acid and pepsin outputs and mucosal blood flow were not correlated with time. 5. The assumed pepsin store during each period was calculated and after 40 min of vagal stimulation there is a constant percentage pepsin output from this assumed store. 6. There is some data to suggest that pepsinogen synthesis was occurring during the period 170-220 min of vagal stimulation. 7. Sympathetic nerve stimulation which started at 160 min after the beginning of sustained vagal stimulation, significantly inhibited gastric acid secretion and mucosal blood flow, and in addition it significantly inhibited pepsin secretion. This is consistent with the hypothesis that sympathetic nerve inhibition of gastric mucosal function is mediated by a vasoconstrictor mechanism.
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PMID:Pepsin secretion in the anaesthetized cat and the effect of sympathetic nerve stimulation. 78 60


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