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)

In five conscious dogs with gastric fistula and two duodenal cannulas, plasma RIA secretin and gastrin levels were determined in response to 1) infusion of 0.1 N HCl in the proximal duodenal cannula, 2) ingestion of a meal, and 3) intraduodenal infusion of 0.1 N HCl following ingestion of a meal. Significant increases in plasma RIA secretin levels occurred during duodenal acidification. However, no significant change occurred in the secretin levels after ingestion of a meal, whereas significant increase in plasma gastrin level was observed. Postprandial duodenal pH remained above 4.5 for 3 h.
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PMID:Plasma secretin and gastrin responses to a meat meal and duodenal acidification in dogs. 0 78

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

Plasma secretin, plasma gastrin and pancreatic bicarbonate output were measured in three healthy youths before and after a 10 min period of duodenal infusion of 50, 75 and 100 ml 100 mmol/1 HCl. Plasma secretin rose to a shortlived peak within 10 min, whereas plasma gastrin fell gradually to values significantly below the basal level 60 min after the start of duodenal acidification. Pancreatic bicarbonate output showed a more sustained increase following duodenal acidification. Significant positive correlations were obtained between plasma secretin and infused dose of HCl, between pancreatic bicarbonate output and infused dose of HCl and between plasma secretin and pancreatic bicarbonate output. The calculated maximal pancreatic bicarbonate output (Vmax) of 30.6 mEq/h and the calculated dose of secretin to elicit half maximal pancreatic bicarbonate output (S50) of 0.2 CU/kg-h following duodenal acidification were comparable to that seen after intravenous infusion of secretin. No significant correlation was found between plasma secretin and plasma gastrin. It is suggested that the pancreatic stimulation subsequent to duodenal acidification is mainly effected by release of secretin, and that the fall in plasma gastrin may be caused by a HCl-induced inhibition of gastrin release from the duodenum.
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PMID:The effect of duodenal acidification on plasma secretin and gastrin and pancreatic bicarbonate secretion in man. 3 87

The significance of antral pH for the basal serum level of immunoreactive gastrin and for the release of gastrin during insulin hypoglycemia has been studied in duodenal ulcer (DU) patients. To permit paired comparisons, 14 DU patients underwent two or three tests with insulin. Venous blood samples were collected at fixed intervals for determination of gastrin (radioimmunoassay). In the first insulin test, the gastric juice was aspirated; in the second test, the stomach was perfused with citrate-phosphate buffer, pH 7.0; and in the third test the stomach was perfused with 0.1M HCl, pH 1.0. The rate of buffer or acid perfusion was adjusted, and the pH of the perfusate was kept above 5.0 and below 1.3, respectively. Gastric perfusion with buffer or acid for 1 hour did not affect the basal serum gastrin level, nor did perfusion with buffer for 3 hours. Insulin hypoglycemia stimulated acid secretion and produced a significant integrated serum gastrin response during gastric aspiration, but the gastrin response was four times greater during buffer perfusion. Acid perfusion abolished the gastrin response. From our previous and present findings, it is concluded that the gastrin in serum during basal conditions is of extra-antral origin and is independent of antral pH. Insulin hypoglycemia releases antral gastrin by a pH-sensitive mechanism in DU patients; the release is suppressed at pH 1.3 or less and also is markedly inhibited when the gastric juice is aspirated.
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PMID:Significance of antral pH for gastrin release by insulin hypoglycemia in duodenal ulcer patients. 4 Mar 12

The effect of variations of intra-antral pH on the intraluminal release of somatostatin was studied. Acute pouches were created in anaesthetized cats, and the pouches were perfused with solutions differing in pH. Somatostatin levels were then measured in the perfusates. In this model phosphate buffer was a potent stimulator of intra-antral somatostatin release, whereas perfusion with 0.1 M HCl failed to release somatostatin by itself. Since phosphate buffer also releases gastrin, the releasing effect ought to be exerted beyond the mechanism that can be blocked by somatostatin. (Thus the stimulatory effect of phosphate buffer might be exerted on the membranes of the endocrine cells.)
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PMID:Phosphate buffer stimulates somatostatin release into the antral lumen of anaesthetized cats. 4 3

Gastric acid secretion, pepsin concentration in gastric juice and acetylcholinesterase and histidine decarboxylase activities in gastric mucosa of rats treated with dichlorvos (DDVP) were investigated. The increase of HCl secretion, the decrease of acetylcholinesterase activity and enhanced activity of histidine decarboxylase were observed. It is suggested that a higher gastric acid secretion is secondary to histamine production in gastric mucosa, induced by acetylcholine yields gastrin yields histidine decarboxylase mechanism.
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PMID:Dichlorvos intoxication and gastric secretion. 11 26

By means of histochemical methods it was established that carboanhydrase of the parietal cells of fundal glands and HCO-3 stimulated ATP-ase of the rat's gastric mucosa capillaries disposed next to the parietal cells were activated by food and histamine. The obtained data confirm the idea of the multicellular functional essembly sustaining HCL secretion (R. I. Salganik, 1974). Should gastrin induce the formation of histamine in endocrinous cells and the histamine activate carboanhydrase in parietal cells, our data confirm the supposition that HCO-3-ions stimulate ATP-ase sustaining the exchange between HCO-3-cells and C1- of blood to form HCl in the endothelial cells of blood capillaries adjacent to the parietal cells.
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PMID:[Histochemical study of carbonic anhydrase and HCO3(-)-stimulated adenosine triphosphatase in the rat stomach during hydrochloric acid secretion]. 13 Aug 54

The regulation patterns of gastric acid secretion in rats were investigated. Pentagastrin and histamine stimulate gastric acid secretion, but the inhibitors of DNA-dependent synthesis of RNA and of proteins prevent only the pentagastrin action. It has been found that pentagastrin induces histidine decarboxylase in gastric mucosa, ensuring local accumulation of histamine. The latter activates adenylate cyclase and results in 3',5'-AMP accumulation in gastric tissues. The administration of pentagastrin, histamine or 3',5'-AMP enhances the activity of gastric carbonic anhydrase, the enzyme which takes part in HCl formation. The data suggest that these three compounds act sequentially (pentagastrin leads to histamine leads to3',5'-AMP) and the effect of the last one could be mediated through 3',5'-AMP dependent protein kinase. The experiments in vitro demonstrated that gastric carbonic anhydrase can be separated into two isoenzymes and thephosphorylation of one of them by the 3',5'-AMP dependent protein kinase sharply increases its activity. The findings raise the possibility that histamine and 3',5'-AMP, mediating gastrin action, form together with enzymes (histidine decarboxylase, adenylate cyclase, protein kinase, carbonic anhydrase) a caascade of amplifiers. Autoradiographic studies have shown that [3H]-pentagastrin is not bound by oxyntic cells but adheres preferentially to histamine-producing alpha-like endocrine cells and to the chief cells, while 3H-histamine adheres preferentially to oxyntic and to chief cells. Electron microscopy indicates that only pentagastrin (but not histamine) initiates in alpha-like endocrine cells ultrastructural changes characteristic for induction. Pentagastrin, histamine and 3',5'-AMP administration produces in oxyntic cells ultrastructural changes typical for the secretion processes. These results lead to assumption that pentagastrin (gastrin) induces histidine decarboxylase in alpha-like endocrine cells of gastric glands. Histamine which is secreted enhances adenylate cyclase activity in the neighbouring oxyntic cells where 3',5'-AMP dependent protein kinase activates carbonic anhydrase by means of phosphorylation. These different cells form, probably, a multicellular functional unit for gastric acid secretion.
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PMID:Integration of biochemical functions of different cells of rat gastric mucosa for hydrochloric acid secretion. 18 10

With combined immunofluorescent, cytochemical and electron microscopic investigations the enterochromaffin cell system has been differentiated into 5 distinct endocrine cell types in the human stomach and into 8 cell types in the intestine. These endocrine cells are probably of neuroectodermal origin and belong to the APUD (amine precursor uptake and decarboxylation)-system. Maximal gastrointestinal hormone concentrations as determined by tissue extracts correlate fairly well to the location of each endocrine cell type in various segments of the gastrointestinal tract. In certain gastroenteropathies the pathophysiological disturbances can be explained by pathomorphological alterations of the disseminated endocrine cells. 1. The gastrin-producing G-cell is the predominating endocrine cell in the gastric antrum. Besides immunocytochemistry the G-cell can be demonstrated with argyrophilic reaction (Grimelius, 1968), masked metachromasia and leadhematoxylin. The ultrastructural features are variable, depending on functional activity. The secretory granules are usually only slightly osmiophilic, measuring 200 till 250 nm in diameter. By some working groups a positive immunofluorescence with gastrin-antisera has been demonstrated in A1- or D-cells of the pancreatic islets. However, numerous negative results have been reported, too. Considering physiological conditions, a gastrin-secretion of the human pancreatic islets has not been secured without doubt. 2. The EC-cell produces serotonin and in the intestine motilin, too. Besides the formaldehyde-induced fluorescence, these cells can be demonstrated with diazonium and argentaffin reactions, less specific with argyrophilic methods. Ultrastructurally the EC-granules are easily differeniated from the other endocrine cells by their pronounced osmiophilia and pleomorphism. In experimental conditions the EC-cells demonstrate species- and site-specific alterations. With reserpine no ultrastructural changes were demonstrable in EC-cells of the rat. However, marked ultrastructural alterations with an increase of the hormone-producing organelle system were noticed after administration of parachlorophenylalanine (PCPA) which interferes with serotonine synthesis; 5. The gastric D-cells are characterized by large secretory granules similar to pancreatic D-cells. They secrete the HCl-inhibitory peptide somatostatin. 4. The D1-cell is a cell type with unknown function. The cytoplasm contains small granules with variable electron density. According to most authors, they represent a distinct cell type and not just a variant of the G-cells. It may be very difficult, however, to separate certain forms of D1-cells from functionally altered G-cells. 5. The A-cell can be found in the gastric mucosa of certain animal species, where it has been demonstrated by immunocytochemistry with antisera to gut-glucagon. This cell type does not occur in the human gastric mucosa. 6...
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PMID:[Pathomorphologic studies of the endocrine cells in the gastrointestinal mucosa. Physiology, cytochemistry and ultrastructure (author's transl]. 19 Aug 18

Somatostatin cells in the stomach of the rat have a characteristic shape and distribution. In the antral mucosa they occur together with gastrin cells and enterochromaffin cells at the base of the glands. In the oxyntic mucosa they are scattered along the entire glands with some predominance in the zone of parietal cells. Throughout the gastric mucosa the somatostatin cells possess long and slender processes that emerge from the base of the cell and end in club-like swellings. Such processes appear to contact a certain proportion of neighbouring gastrin cells in the antral mucosa and parietal cells in the oxyntic mucosa. Exogenous somatostatin given by intravenous infusion to conscious rats counteracted the release of gastrin stimulated by feeding, elevated antral pH or vagal excitation. Gastrin causes parietal cells to secrete HCl and endocrine cells in the oxyntic mucosa to mobilise and synthesise histamine. Somatostatin is known to block the respone of the parietal cells to gastrin. In contrast, somatostatin did not block the response of the histamine-storing endocrine cells to gastrin, perhaps because these endocrine cells lack receptors to somatostatin. Conceivably, somatostatin in the gastric mucosa has a paracrine mode of action. The observations of the present study suggest that somatostatin may affect some, but not all of the various cell types in the stomach. Under physiological conditions this selectivity may be achieved in the following ways: 1) Communication may be based on direct cell-to-cell contact. 2) Only certain cell types are supplied with somatostatin receptors.
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PMID:Topography of somatostatin cells in the stomach of the rat: possible functional significance. 22 55


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