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)

1. Pentagastrin stimulated gastric acid and pepsin secretions show parallel rates of tachyphylaxis in the conscious cat. The responses to histamine show only slight tachyphylaxis. 2. Somatostatin 10 microng.kg(-1).hr(-1) inhibits pentagastrin but not histamine stimulated acid secretion and inhibits pentagastrin stimulated pepsin secretion. 3. The inhibition of pentagastrin stimulated acid and pepsin secretion by Somatostatin delays the tachyphylaxis of these responses, but the rates of tachyphylaxis when they do subsequently occur are identical. 4. Metiamide 10 mg-kg(-1)-hr(-1) equally inhibits histamine and pentagastrin stimulated acid secretion but does not inhibit pentagastrin stimulated pepsin secretion. 5. Inhibiton of acid secretion during metiamide infusion neither prevents nor delays acid nor pepsin tachyphylaxis. 6. It is suggested that tachyphylaxis of acid and pepsin secretion is a gastrin receptor phenomenon and that Somatostatin occupies or modifies the behaviour of these receptors, preventing tachyphylaxis. Metiamide, however, exerts its action only on the histmine H2-receptor and not the gastrin receptor mechanism, and this apparently does not prevent or delay acid tachyphylaxis.
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PMID:The effects of somatostatin and metiamide on tachyphylaxis of pentagastrin stimulated gastric acid and pepsin secretion in the conscious cat. 32 96

In conscious cats with chronic gastric and pancreatic fisulas, the effect of somatostatin (GH-RIH) on gastric and pancreatic secretion and peptic ulcer formation was examined. GH-RIH infused intravenously in graded doses (range: 0.62 to 5.0 microng/kg-hr) inhibited dose-dependently gastric acid response to pentagastrin but failed to affect acid response to histamine. GH-RIH caused a marked inhibition of pepsin secretion induced by both pentagastrin and histamine and decreased pancreatic bicarbonate but not protein response to exogenous secretin or intraduodenal acid. It effectively prevented the formation of duodenal ulcers produced by prolonged administration of both pentagastrin or histamine.
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PMID:Effect of somatostatin on gastrointestinal secretions and peptic ulcer production in cats. 32 38

1. Somatostatin, 10 microgram kg-1 hr-1, inhibited gastric acid and pepsin secretion stimulated by pentagastrin, 8 microgram kg-1 hr-1, in conscious and anaesthetized cats with chronically implanted gastric fistulae. In the acutely surgically prepared anaesthetized cat, Somatostatin inhibited pepsin secretion but produced little inhibition of gastric acid secretion or mucosal blood flow. 2. Secretin stimulated pancreatic juice volume was not significantly reduced in acutely prepared anaesthetized cats, but there was a limited reduction of cholecystokinin-pancreozymin stimulated pancreatic amylase secretion and gall bladder contraction. 3. Somatostatin had neither stimulatory nor inhibitory effects on electrolyte and amylase secretion in the isolated saline-perfused cat pancreas. 4. The results suggest that some of the effects of Somatostatin may depend on the interaction on the target cell of other factors, nervous or humoral which may vary in different experimental preparations.
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PMID:Comparison of the effect of somatostatin on gastrointestinal function in the conscious and anaesthetized cat and on the isolated cat pancreas. 33 Aug 38

The effect of somatostatin, a growth hormone releasing-inhibiting hormone (GH-RIH) on basal and meal-, pentagastrin-, or histamine-stimulated gastric acid and pepsin secretion was studied in six duodenal ulcer patients. Intravenous GH-RIH infused in graded doses ranging from 0.62 to 5.0 microgram/kg/hr produced a dose-related inhibition of pentagastrin-induced acid secretion reaching about 15% of control level at the dose of 5.0 microgram/kg/hr. Acid inhibition was paralleled by a decrease in the pepsin output and accompanied by a dose-dependent reduction in serum growth hormone and insulin levels measured by radioimmunoassay. GH-RIH used in a single dose of 2.5 microgram/kg/hr produced about 85% inhibition of acid secretion induced by a meal (measured by intragastric titration) accompanied by a significant decrease in serum gastrin and insulin levels. The effect of GH-RIH on histamine-stimulated secretion was very modest and observed only after stopping the GH-RIH infusion. Thus GH-RIH suppressed acid and pepsin secretion induced by pentagastrin and a meal, and this effect was accompanied by a suppression of serum growth hormone and gastrin levels which may contribute to the inhibition of gastric secretion observed.
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PMID:Effect of somatostatin on meal-induced gastric secretion in duodenal ulcer patients. 33 84

Three experiments were carried out in each of 6 healthy students on separate days, in a randomized order. Intravenous saline infusions were given for one hour basally in each experiment. During the second hour either pentagastrin, pentagastrin and somatostatin, or somatostatin alone were given. Gastric juice was collected continuously during all experiments. Somatostatin decreased the volume of gastric secretion and the concentrations of acid and pepsin, and output of acid, pepsin, and intrinsic factor (IF). The plasma gastrin concentration was not changed by somatostatin. A rebound effect was seen on pepsin and IF outputs after cessation of somatostatin, and on blood sugar concentration. The present study suggests that somatostatin acts on gastric secretion either directly or by mechanisms other than by inhibition of gastrin. The rebound of pepsin and IF indicates a release-inhibiting action on these substances similar to the effect of somatostatin on the release of some hormones.
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PMID:The effect of somatostatin on pentagastrin-stimulated gastric secretion and on plasma gastrin in man. 33 22

The effect of a small dose of somatostatin (0.05 mg/h) on the gastric secretion of acid, pepsin and Intrinsic Factor (IF) after stepwise increases in the dose of pentagastrin was examined in six healthy volunteers. The gastric secretion of acid, pepsin and IF in response to pentagastrin was significantly reduced by a continuous infusion of somatostatin. The pattern of inhibition indicates that somatostatin is a competitive inhibitor of pentagastrin in the stimulation of gastric secretion of both acid, pepsin and IF. This finding supports the hypothesis of a direct effect of somatostatin on the exocrine secretory cells of the stomach.
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PMID:A small dose of somatostatin inhibits the pentagastrin stimulated gastric secretion of acid, pepsin and intrinsic factor in man. 34 47

1. The effect of somatostatin and eighteen somatostatin analogues on pentagastrin-stimulated gastric acid and pepsin secretion was investigated in the conscious vagotomized cat prepared with chronic gastric fistulae. The majority of the analogues are peptides where D-amino acids are incorporated into the molecule instead of the natural L-isomers. 2. The ID50 for cyclic-somatostatin inhibition of near-maximal gastric acid secretion stimulated by pentagastrin 8 microgram kg-1 hr-1 was found to be 1.29 +/- 0.13 n-mole kg-1 hr-1. Pentagastrin-stimulated pepsin secretion had a lower threshold to somatostatin inhibition than did acid secretion. 3. D-Phe6, D-Phe7, D-Thr10, D-Thr12 and D-Phe6-D-Trp8 analogues all show low biological activity against the secretion of gastric acid and pepsin, growth hormone, insulin and glucagon. None of these analogues are antagonists of the cyclic-somatostatin inhibition of gastric secretion, suggesting that they have low affinity for this somatostatin receptor. 4. The analogues under investigation show parallel changes in activity against gastric and growth hormone secretion, suggesting a similarity between the gastric and growth hormone receptors for somatostatin. 5. D-Cys14 analogues are equipotent with or have a greater potency than cyclic-simatostatin in inhibiting the secretion of gastric acid, growth hormone and glucagon but show low insulin inhibiting activity.
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PMID:Structure-activity relationships of eighteen somatostatin analogues on gastric secretion. 34 35

Somatostatin inhibition of gastric acid and pepsin secretion stimulated by insulin-hypoglycaemia was quantified in six conscious cats prepared with cannulated gastric fistulae. Somatostatin 0.5-5 microgram kg-1h-1 produced a dose dependent reduction of both acid and pepsin secretions stimulated by insulin 0.2 u kg-1h-1. The doses of somatostatin which produced 50% inhibition of pepsin and acid secretions (ID50) were not significantly different (0.70 +/- 0.16 and 0.93 +/- 0.11 microgram kg-1h-1 respectively). The slope of the calculated correlation line relating % inhibition of pepsin and % inhibition of acid is within experimental error of unity indicating equality of action of somatostatin on insulin-stimulated acid and pepsin secretion. The results indicate that somatostatin is a more potent inhibitor of insulin 0.2 u kg-1h-1 stimulated acid secretion than pentagastrin 8 microgram kg-1h-1 stimulated acid secretion, but is a more potent inhibitor of pentagastrin--than insulin--stimulated pepsin secretion. As insulin stimulates less acid and more pepsin secretion than pentagastrin, the differences in sensitivities to somatostatin of these secretions produced by the two stimulants is thought to be a result of the different absolute amounts of secretion produced by the stimulants.
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PMID:Quantitation of somatostatin inhibition of insulin-stimulated gastric acid and pepsin secretion in the cat. 35 81

The effect of somatostatin on pentagastrin-induced gastric secretion was assessed on 6 isolated canine stomachs perfused ex vivo with homologous blood. Hormones were given at a constant rate into the gastric arterial circulation. Somatostatin caused inhibition of the HCl concentration and output and reduced the secretion volume in all stomachs studied. The output but not the concentration of pepsin was also reduced.
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PMID:Effect of somatostatin on pentagastrin stimulated secretion by isolated canine stomachs, perfused ex vivo with homologous blood. 35 28

The chemistry, localisation, release and effects of gastrointestinal hormones and some related peptides are surveyed. Their main presumed physiologic actions are: gastric acid and pepsin secretion are stimulated by gastrin and to a less degree by secretin. Acid secretion is inhibited by bulbo-enterogastrone and GIP. Biliary water and electrolytes are augmented by gastrin, CCK-PZ, secretin and VIP and inhibited by Substance P. Pancreatic bicarbonate and enzyme secretions are stimulated by secretin and CCK-PZ, especially in combination. Lower oesophageal and antral motility and tonus are elevated following gastrin and motilin; the gallbladder and small intestine empty following CCK. Gastrin regulates gastrointestinal, and CCK pancreatic, tissue growth. Somatostatin inhibits all gut hormones. All peptides are vasoactive within the splanchnic area, each one in a specific manner.
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PMID:Gastrointestinal hormones. 35 98


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