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 effects of vagal stimulation on gastric secretion and on blood gastrin, histamine and somatostatin release have been assessed in three esophagostomized dogs equipped with gastric fistula and Heidenhain pouch. The animals were submitted to sham feeding of variable duration (from 2.5 to 12.5 min) and composition. In response to standard composition of the sham feeding, acid and pepsin responses were observed in the gastric fistula only; they were closely related to the sham feeding duration. Integrated histamine responses were also closely related to sham feeding duration and were correlated with acid or pepsin responses. Gastrin was released by sham feeding induced-vagal stimulation, but there were no relationship between gastrin and secretory responses. Somatostatin release decreased as duration of sham feeding stimulation increased and correlated negatively with acid or pepsin responses. Modified standard sham feeding, by adding either lipids or glucids resulted in the same gastric and hormonal responses as standard sham feeding. It appears that 1 degree) vagal stimulation resulting in the psychosensorial receptors stimulation can be quantified, 2 degrees) histamine reduces somatostatin release and could represent a non cholinergic vagal mediator, capable of controlling somatostatin release in the cephalic phase of gastric secretion.
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PMID:[Psychosensory initiation of gastric secretion in dogs. Inter-relation of vagal component, gastrin, histamine and somatostatin]. 247

The heterogeneity of muscarinic receptors has been well supported by differential characteristics between pirenzepine and atropine both in receptor binding and in whole tissue pharmacology studies. Under these conditions pirenzepine has been classified as a selective receptor antagonist with high affinity for M1 receptors. The antisecretory properties of pirenzepine on gastric acid and pepsin secretion may be attributed to the antagonistic activity of the drug on muscarinic M1 receptors of gastric intramural plexuses, whereas the effect on parietal muscarinic M2 receptors seems of less importance. Additional inhibitory mechanisms on gastric secretion may be represented by pirenzepine-induced increase in somatostatin release from gastrointestinal system. Significant cytoprotective properties of pirenzepine have been observed on a variety of experimentally induced peptic ulcerations. This protective activity may be due to pirenzepine-induced increase in gastric mucosal blood flow as well as to the increase in gastric transmural electric potential difference. In accordance with this pharmacodynamic profile of pirenzepine, numerous clinical studies have revealed its efficacy in the treatment of both duodenal and gastric ulcerations. In addition to this, the clinical usefulness of the drug has been demonstrated in Zollinger-Ellison syndrome, in stress ulceration, in acute gastrointestinal bleeding as well as in gastritis, duodenitis and non-ulcer dyspepsia. In most of the studies pirenzepine has been found to be well tolerated with a low incidence of antimuscarinic effects which may occur at salivary, ocular, cardiac and urinary sites. The clinical use of pirenzepine alone or in association with H2 blockers is recommended in the treatment of peptic ulcer patients, in the case of acute gastrointestinal haemorrhage and in patients non responders to H2 antagonists.
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PMID:[A selective antimuscarinic agent: pirenzepine. Review of its pharmacologic and clinical properties]. 257 37

This study was designed to compare gastric antisecretory effects of telenzepine, a new antimuscarinic agent, with those of pirenzepine and atropine in dogs. None of these antimuscarinics affected gastric acid secretion induced by histamine but all of them caused a dose-dependent inhibition of acid secretion from the gastric fistula (GF) and Heidenhain pouches (HP) stimulated by pentagastrin and bethanechol, telenzepine being 5-9 times more potent than pirenzepine and equipotent with atropine. All antimuscarinics were also effective inhibitors of acid responses to sham feeding and ordinary feeding. The inhibitory effect of telenzepine and pirenzepine were not accompanied by any major alterations in plasma gastrin or somatostatin but those of atropine were related to significant increase in plasma gastrin and to significant decrease in plasma somatostatin levels, suggesting the involvement of M2 receptors in the cholinergic control of these hormones. All three antimuscarinics were effective inhibitors of pepsin secretion induced both from the GF and HP by all secretagogues used. Neither telenzepine nor pirenzepine administered in various doses affected the heart rate while atropine caused a significant increase in heart rate confirming that the former agents are selective M1 receptor antagonists. This study provides evidence that telenzepine is more potent than pirenzepine in the inhibition of gastric secretion induced by pentagastrin, bethanechol, sham-feeding and ordinary feeding and that, unlike atropine, it does not increase plasma gastrin responses to meat feeding. In fact, telenzepine and pirenzepine alike reduced plasma gastrin concentrations under these conditions. No influence of these antimuscarinics on plasma somatostatin levels was observed.
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PMID:Comparison of telenzepine, pirenzepine and atropine on gastric acid and pepsin secretion in response to histamine, pentagastrin, bethanechol, sham-feeding and feeding. 257 51

The effect of bombesin (BBS) and gastrin releasing peptide (GRP) on gastric emptying was studied in conscious cats. This effect was measured simultaneously with antral motility. Acid and pepsin secretions as well as blood hormonal peptide release were additionally measured. A dual effect was observed. First, BBS and GRP slowed gastric emptying of liquids, while antral motility was decreased, then after 60 minutes of continuous intravenous infusion, antral motility returned to basal values and gastric emptying effect reversed. The mechanism of this peculiar action is independent of gastrin, pancreatic polypeptide, somatostatin and motilin release and most probably connected with a cholinergic stimulation induced by the peptides, the late predominance of which counterbalances the inhibitory effect of bombesin-like peptides on antral motility.
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PMID:Dual effect of bombesin and gastrin releasing peptide on gastric emptying in conscious cats. 275 71

Mice were injected 3 times a day for 12 days with 8 micrograms/kg of somatostatin 14 which caused a hypoplasia of parietal and goblet cells, a hypotrophy and hypofunctionality of pancreatic acinar cells with a decrease in lipase and chymotrypsin activities, a decrease in the secretory fuction of the Brunner gland and in the number of dark granules of G cells. Neither villous and microvillous areas nor brush border hydrolase activities were affected. The number of peptic cells and Paneth cells increase as the level of pepsin and lysozyme. Mice were injected 4 times per hour with 2 micrograms/kg of somatostatin. 2 h after the first injection of somatostatin and 90 min after a single injection of tritiated thymidine, fundic, antral, jejunal and ileal labelling indexes strongly decrease (maximal effect in ileum). The inhibitory effect of somatostatin on the digestive epithelial cell proliferation compared to its long-term action only directed on specific cell types evokes probable compensatory mechanisms induced to maintain the equilibrium of the digestive epithelia.
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PMID:Long-term effect of somatostatin 14 on mouse stomach, antrum, intestine and exocrine pancreas. 285 47

The inhibitory activities of somatostatin and PGE2 against pentagastrin-stimulated gastric acid and pepsin secretions were investigated, with and without pretreatment with the cyclooxygenase inhibitor indomethacin, in conscious cats prepared with gastric fistulae. Somatostatin was a potent inhibitor of acid secretion in both vagus intact and vagotomized animals, and its effect was not diminished by indomethacin pretreatment. Somatostatin inhibition of pepsin secretion was diminished after indomethacin, but a similar effect was noted with exogenous PGE2, suggesting a mechanism unrelated to inhibition of prostaglandin synthesis. It is concluded that there is no evidence to implicate endogenous prostaglandins in somatostatin inhibition of feline gastric exocrine secretions.
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PMID:Evidence against prostaglandin-mediation of somatostatin-inhibition of gastric secretions. 285 41

The effect of somatostatin on pepsin secretion was determined in six dogs with gastric fistulas during stimulation with bethanechol. Somatostatin inhibited dose-dependently the stimulated pepsin secretion, with a dose of 0.3 micrograms/kg/h being 35% inhibitory during stimulation with bethanechol, 80 micrograms/kg/h. Continuous infusion of somatostatin for 3 h did not cause any signs of tachyphylaxis. Withdrawal of somatostatin produced a return to the control level. The dose-response kinetics with five doses of bethanechol with and without somatostatin showed inhibition of a noncompetitive type. The effects of somatostatin were not altered by using adrenergic, dopaminergic, or serotonergic blocking drugs.
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PMID:Effect of somatostatin on bethanechol-stimulated gastric pepsin secretion in gastric fistula dogs. 285 51

The effects of antramine, an antral histamine (AH), and of synthetic histamine (SH) on acid, pepsin, and gastrin responses to meals alone or in combination with somatostatin were studied in dogs equipped with a Heidenhain pouch. Food-induced acid secretion was potentiated by AH and only slightly increased by SH. Pepsin secretion was increased by AH and decreased by SH. Both AH and SH suppressed the inhibitory activity of somatostatin on food-induced secretion. AH potentiated gastrin response to feeding but decreased it when somatostatin was added to the meal. Since acid secretion was unrelated to gastrin response, it would appear that the secretory effects of AH involve a direct action on secreting cells, itself based on the suppression of somatostatin inhibition. Gastric secretion is probably related to gastrin efficacy on secreting cells, which would result from the antagonistic effects of somatostatin and AH. These data suggest an alternative hypothesis concerning the role of histamine in the control of gastric secretion.
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PMID:Antramine (antral histamine) antagonizes somatostatin inhibition on endogenous gastrin-induced gastric secretion. A new hypothesis for the role of histamine in gastric secretion regulation. 286 68

Thirteen male patients with a history of duodenal ulcer were given 150 mg RP 40 749 or placebo tablets at bedtime in a double-blind crossover study. The medication was given for two periods of 10 days with an 11-day wash-out period between. pH and pepsin concentrations were determined each hour in aspirates of gastric juice for 24 h on day 1, 10, 22, 31, and a 2-h collection of gastric juice was examined in the middle of the treatment and wash-out periods. At defined hours blood samples were examined for gastrin, somatostatin, and pancreatic polypeptide (PP) by radioimmunological methods, and concentrations of RP 40 749 were determined in blood and gastric juice. Meals were served at fixed hours on days 1, 10, 22, and 31. After treatment with RP 40 749 a highly significant elevation of pH was found after the 1st day compared with placebo, most pronounced during night hours. The pepsin activity was slightly elevated. The serum concentrations of gastrin were increased and those of somatostatin and PP decreased during the first 3-4 h after medication, with a subsequent normalization. No side effects were observed.
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PMID:The antisecretory effects of RP 40 749 in patients with previous duodenal ulcer. 286 98

In the rat, both partial resection of the pancreas and occlusion of the side branches of the biliodigestive duct were investigated with respect to their influence on gastric secretion (acid, pepsin, sodium), gastric mucosal blood flow (MBF), development of gastric ulcers, and gastrin and somatostatin in the blood. On the 14th postoperative day the exocrine pancreatic function is reduced and ulcer index and severity are significantly enhanced. There are no simultaneous changes in gastric secretion or MBF. Aortal gastrin was decreased and somatostatin was unchanged. We conclude that: in the rat, reduction of exocrine pancreatic function should be considered an ulcerogenic factor; factors others than gastric hypersecretion or reduced MBF are responsible for ulcer formation, and an etiological role of either circulating gastrin or somatostatin is doubtful.
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PMID:Pancreatic surgery, gastric secretion and ulcers in the rat. Increased ulcer development following pancreatic half resection or duct occlusion. 286 8


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