Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of low concentrations of sodium taurocholate on the secretory and electrical activity of isolated rabbit fundic mucosa has been studied. Fundic mucosa maintained a stable potential difference (10.2 +/- 0.6 mV, n = 70) and electrical resistance (85 +/- 6 omega . cm-2, n = 70) and the majority of preparations spontaneously secreted acid (2.85 +/- 0.31 mumol . cm-2 . h-1, n = 70). Histamine (10(-5) and 10(-4) M) and carbachol (10-4 M) increased acid secretion, and these responses were prevented by cimetidine (10(-3) M) and atropine (10(-5) M), respectively. Mucosal application of taurocholate (10(-4) and 10(-3) M) increased net acidity without altering electrical activity. This response exhibited tachyphylaxis, was not altered by pretreating the tissues with cimetidine (10(-3) M), atropine (10(-5) M), or somatostatin (10(-6) M), and occurred in mucosas maximally stimulated by histamine. Sodium thiocyanate (6 x 10(-2) M, serosal side) inhibited spontaneous acid secretion revealing net alkalinization (0.83 +/- 0.05 mumol . cm-2 . h-1, n = 58) that was completely inhibited by anoxia and potassium cyanide (10(-2) M) and markedly reduced by 2,4-dinitrophenol (10(-4) M). Some fundic preparations spontaneously secreted alkali (1.20 +/- 0.20 mumol . cm-2 . h-1, n = 6) after an initial period of acid secretion. Mucosal-side taurocholate (10(-3) M) converted net alkali secretion by both thiocyanate-treated and spontaneously-secreting mucosas to acid secretion without affecting electrical conductance. These secretory responses may be implicated in the pathogenesis of gastric mucosal damage by bile salts.
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PMID:Studies of acid and alkaline secretion by rabbit gastric fundus in vitro: effect of low concentrations of sodium taurocholate. 612 66

After various types of sympathectomy (surgical, chemical, isolated adrenodemedullation; AMX, combined procedures) in the rat, basal gastric secretion, gastric mucosal blood flow (MBF), associated glucose and a variety of hormones in the blood were measured. With the exception of the ineffective surgical sympathectomy, all the other forms variously influence gastric secretion qualitatively (volume, acidity, pepsin) and quantitatively (output per unit time). Chemical sympathectomy has an augmenting effect both on acid (volume, acidity, output) and on pepsin. In general the MBF parallels acid, but the MBF is decreased after AMX despite stable or increased gastric secretion. Sympathectomy, except procedures involving AMX or AMX + surgical sympathectomy, increases spontaneous gastric mucosal lesions. With AMX glucose is diminished, but is elevated following surgical and chemical sympathectomy. Gastrin, insulin and somatostatin are always higher than in sham-operated controls, glucagon after surgical sympathectomy only. It is concluded that (1) the sympathoadrenal system in the rat modulates both basal gastric secretion and blood hormones; (2) the adrenal medulla may participate in the control of gastric MBF, and (3) gastric mucosal lesions are not correctly reflected by the ration MBF/acidity.
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PMID:Basal gastric secretion, mucosal blood flow and associated fasting blood hormones in the rat. Effects of various forms of sympathectomy. 612 14

After vagotomy (truncal, highly selective, superselective) in rats, basal gastric secretion, gastric mucosal blood flow, associated fasting blood glucose and a variety of hormones were measured. All forms of vagotomy reduce acid (volume, acidity, output), but highly selective and superselective--though not truncal--procedures stimulate basal pepsin secretion, whereas mucosal blood flow roughly parallels acid production. Spontaneous gastric mucosal lesions increase after highly selective vagotomy. Both highly selective and superselective--but not truncal--vagotomy tend to increase plasma glucose and somatostatin, while only the former reduces insulin and glucagon. Common to all vagotomies is the development of virtually undetectable calcitonin (less than 25 pg/ml) and of hypergastrinemia. It is concluded that in the rat with draining gastric fistula in response to vagotomy there are moderate differences in regard to gastric mucosal ulcer index, gastric secretion, glucose, glucose-regulating hormones, while lowered calcitonin may be a general feature of low vagal tone.
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PMID:Basal gastric secretion, mucosal blood flow and associated fasting blood hormones in the rat. Effects of various forms of vagotomy. 612 15

Helicobacter pylori infection may be associated with duodenal ulcer (DU) and accompanied by enhanced gastrin release but the mechanism of this H pylori related hypergastrinaemia in DU patients is unclear. Cholecystokinin (CCK) has been implicated in the feedback control of gastrin release and gastric acid secretion in healthy subjects. This study therefore investigated if CCK participates in the impairment of postprandial gastrin release and gastric secretion in six DU patients. Tests were undertaken with and without elimination of endogenous CCK by loxiglumide, a selective CCK-A receptors antagonist, before and after eradication of H pylori with triple therapy (omeprazole, amoxicyllin, bismuth). In H pylori positive DU patients, the post-prandial decline in pH (with median pH 3.5) was accompanied by a pronounced increment in plasma gastrin but the administration of loxiglumide did not affect significantly this postprandial rise in plasma gastrin and gastric pH profile. After eradication of H pylori, the plasma gastrin concentration was reduced while the median postprandial pH was significantly increased (median pH 4.3). The administration of loxiglumide resulted in significantly greater increase in postprandial plasma gastrin and greater decrease in pH (median pH 3.1) in these patients. This study shows that (a) infection with H pylori is accompanied by an enhanced gastrin release and gastric acidity in DU patients, (b) the failure of loxiglumide to affect plasma gastrin or gastric acid secretion in H pylori infected DU patients could be attributed, at least in part, to the failure of endogenous CCK to control gastrin release and gastric secretion by releasing somatostatin, and (c) the test with loxiglumide may be useful in the identification of patients with impaired feedback control of gastrin release and gastric secretion resulting from infection with H pylori.
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PMID:Eradication of Helicobacter pylori restores the inhibitory effect of cholecystokinin on postprandial gastrin release in duodenal ulcer patients. 748 32

The patients with chronic superficial gastritis were perfused in the stomach with 20 g of Dendrobium nobile to observe the variations in gastric acidity output, serum gastrin and plasma somatostatin concentration. The result showed a significant increase in both acidity output and serum gastrin concentration (P < 0.01). No significant change occurred in plasma somatostatin concentration (P > 0.05).
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PMID:[Effect of Dendrobium nobile Lindl. on gastric acid secretion, serum gastrin and plasma somatostatin concentration]. 764 85

Somatostatin is an endogenous cyclic tetradecapeptide which can exert effects on a wide range of gastrointestinal functions, including gastric acid and pepsin secretion, gastric and small intestinal motility, splanchnic blood flow, pancreatic enzyme secretion, intestinal nutrient absorption and gallbladder contractility. Somatostatin has also been shown to reduce the severity of ethanol-induced gastric damage. In this study, we examined the effect of pretreating rats with somatostatin (s.c.) on susceptibility to gastrointestinal damage induced by hemorrhagic shock, stress, platelet-activating factor (PAF), indomethacin or endotoxin. Somatostatin significantly reduced the extent of gastric damage induced by hemorrhagic shock when given at a dose of 20 micrograms/kg or greater (P < 0.05). Somatostatin (20-50 micrograms/kg) also had a dose-dependent protective effect against stress-induced gastric damage. Versus gastric damage induced by intravenous PAF, a dose of 5 micrograms/kg of somatostatin had no effect, while doses of 15-100 micrograms/kg significantly reduced the extent of injury to the stomach. In contrast, somatostatin had no significant effect on gastric or intestinal damage caused by intravenous administration of Salmonella enteritidis endotoxin or by oral administration of indomethacin, despite significantly and dose-dependently (2-10 micrograms/kg) reducing both the volume and titratable acidity of gastric secretion. A protective dose of somatostatin (20 micrograms/kg) had only a small and transient effect on gastric blood flow. The present results demonstrate the effectiveness of somatostatin in protecting the mucosa from injury in a variety of models, and suggest that inhibition of gastric acid secretion is not the sole mechanism underlying these protective effects.
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PMID:Protective effects of somatostatin against gastric damage induced by hemorrhagic shock, stress and PAF in the rat. 790 73

The patients with chronic superficial gastritis were selected in the study. The variation in gastric acidity output, serum gastrin and plasma somatostatin concentration were observed during the Saussurea lappa decoction (SLD) perfusion into the stomach. There was no significant changes in acidity output, serum gastrin and plasma somatostatin concentration after the perfusion of SLD (P > 0.05). Changes in gastric emptying and plasma motilin concentration were observed after oral administration of the SLD in 5 healthy volunteers. The time of gastric emptying was markedly shortened after oral administration of SLD (P < 0.01). A significant increase occurred in plasma motilin concentration at 30 min. after oral administration of SLD (P < 0.01). It revealed that SLD could accelerate the gastric emptying and increase the endogenous motilin release.
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PMID:[Effect of Saussurea lappa on gastric functions]. 795 Feb 25

CCK8 is a poor stimulant of gastric acid secretion in vivo, but is equipotent to gastrin-17 (G17) in in vitro systems. To further evaluate the role of cholecystokinin (CCK) in regulating acid output in humans, dose-response curves were constructed to CCK8 or G17 (6.4-800 pmol kg-1 per h) with and without a specific CCK-A receptor antagonist (loxiglumide). During loxiglumide infusion, G17-stimulated acid output was unchanged, whereas CCK8-stimulated secretion increased significantly. Gastric somatostatin-14 release increased fivefold with CCK8 alone, but was blocked with loxiglumide administration. These data suggest that CCK8 directly stimulates acid secretion by binding to a CCK-B/gastrin receptor on parietal cells, but at the same time inhibits acid responses by stimulating gastric somatostatin release to a CCK-A receptor-mediated pathway. To test which action of CCK is relevant under physiological circumstances, the effect of loxiglumide on fasting and post-prandial acidity was measured through continuous pH-metry. After eating, gastrin levels increased fourfold compared to controls with concomitant increases in acid secretion. These results suggest that post cibum, CCK is an inhibitor of acid secretion by regulating gastrin through local somatostatin; they support the hypothesis that CCK acts as an enterogastrone.
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PMID:Cholecystokinin is a physiological regulator of gastric acid secretion in man. 795 87

The activity of gastric parietal cells in terms of hydrochloric acid (HCl) secretion is regulated by the interaction of stimulatory substances (e.g. gastrin) and inhibitors (e.g. somatostatin) acting in an endocrine and paracrine mode, as well as luminal factors. In the present study the following parameters were measured: the synthesis (mRNA), storage (tissue peptide concentration) and secretion (plasma peptide concentration) of somatostatin and gastrin following short-term treatment of rats with pentagastrin (acid stimulant), secretin, omeprazole (reduces gastric acidity by inactivating gastric H/K ATPase) and the somatostatin analogue octreotide (reduces gastric acidity by inhibiting both the parietal cell and gastrin). The mRNA coding for H/K ATPase and carbonic anhydrase II (CA II), the two enzymes responsible for the generation of hydrogen ions from the parietal cell, were also quantitated. In response to octreotide, somatostatin peptide and mRNA levels in the fundus rose to 180 +/- 16% (P < 0.001) and 1073 +/- 356% (P < 0.05) of control, respectively. In contrast, octreotide caused a decrease in antral somatostatin peptide and its mRNA did not change significantly. No significant changes in synthesis, secretion or storage of gastrin were observed except for omeprazole induced hypergastrinaemia (580 +/- 76%, P < 0.001). H/K ATPase and CA II mRNA were largely unaffected except for an increase in CA II mRNA following octreotide and a decrease in H/K ATPase mRNA after pentagastrin. These data support the concept of the differential control of antral and fundic somatostatin synthesis and provide evidence for a regulatory loop by which somatostatin can influence its own synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Secretory and biosynthetic responses of gastrin and somatostatin to acute changes in gastric acidity. 852 6

The effect of 24-hours continuous somatostatin-14 infusion on the volume of the bile secretion and on the bile composition were studied in seven patients with malignant biliary obstruction who had transhepatic external biliary drainage. The bile acid composition was measured with high performance liquid chromatography (HPLC). Somatostatin infusion significantly reduced the daily bile loss from median 473 ml to 140 ml (41 per cent, p = 0.01) with a concomitant significant reduction in the daily molar loss of cholesterol, triglyceride, Na+, K+, Cl-, Ca+2 and Mg+2. The loss of chloride and sodium was reduced with median 50 mmol/day each (p = 0.01). The relative concentrations of the measured bile constituents did not change significantly, except for bile acids (p = 0.02): the concentration of glycochenodeoxycholic acid increased significantly (p = 0.04). The molar loss of taurocholic acid decreased significantly (p = 0.035), so the increased concentration of glycochenodeoxycholic acid resulted only in a marginally significant reduction in the total molar loss of bile aids (p = 0.051). Somatostatin is a potent inhibitor of bile secretion. The peptide may be used in severely bile depleted patients for reducing their serious electrolyte and acidity problems. Analysis of bile acid composition by HPLC is well suited for further investigations of the regulatory mechanisms of bile acid secretion.
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PMID:Somatostatin reduces bile secretion and loss of bile constituents in patients with external biliary drainage. 880 84


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