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)

Hypercalcemia produced in healthy volunteers by intravenous infusions of calciumgluconolactobionate increased outputs of gastric acid, pepsin, and pancreatic enzymes. Hypercalcemia did not affect gallbladder emptying and serum gastrin values. Further, intravenous somatostatin (SRIF, 5 micrograms/kg.h) markedly inhibited secretion of gastric acid (p less than 0.01), pepsin (p less than 0.05), and pancreatic enzymes (p less than 0.02) stimulated by hypercalcemia. SRIF-inhibited outputs were below basal values. These results indicate that the inhibitory effect of SRIF on exocrine cells of the human gastrointestinal tract can not be reversed by extracellular hypercalcemia.
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PMID:[Effect of somatostatin on hypercalcemia stimulated gastric juice and exocrine pancreas secretion in the human]. 287 May 92

The effects of somatostatin on gastric mucosal blood flow (GMBF), acid secretion, and pepsin secretion were evaluated. Conscious gastric fistula dogs were used, with neutral red clearance as the method for estimating the mucosal blood flow. Somatostatin inhibited the pentagastrin- and bethanechol-stimulated gastric acid and pepsin secretion and resulted in an absolute decrease in mucosal blood flow. The ratios between GMBF and secretion (acid and pepsin) were increased during somatostatin infusion, which suggests a relative increase in mucosal blood flow and independent inhibition of gastric secretion. It may be concluded from this study that the acid- and pepsin-inhibitory effects of somatostatin are not mediated by changes in the GMBF.
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PMID:Somatostatin increases the ratio between gastric mucosal blood flow and gastric acid and pepsin secretion in dogs. 287 16

The role of prostaglandins in somatostatin mediated gastric inhibitory effects has been investigated in conscious cats. The effect of somatostatin on pentagastrin-, insulin- and histamine plus bethanechol-stimulated gastric acid and pepsin secretion was determined with and without indomethacin pretreatment. Somatostatin significantly inhibited acid and pepsin secretion and this effect was not diminished by cyclo-oxygenase inhibition. It is concluded that there is no evidence that endogenous prostaglandins mediate the inhibitory effects of somatostatin on gastric acid and pepsin secretion in the cat.
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PMID:Are prostaglandins involved in somatostatin mediated inhibition of gastric secretion in the cat? 287 23

The purpose of the present study was to evaluate whether the inhibitory effects of beta-adrenergic agonists on gastric secretory activity in vivo could be mediated through a local release of somatostatin. The gastric secretion was measured during continuous stimulation with pentagastrin (1 microgram/kg/h). The infusion of isoprenaline (beta 1 + beta 2), salmefamol (beta 2), and somatostatin produced inhibitory effects on both acid and pepsin secretion. The reaction patterns were similar for isoprenaline and somatostatin, whereas salmefamol induced an inhibition of longer duration and with dissimilar dose-response kinetics. The gastric somatostatin release was significantly increased after infusion of both beta-adrenergic agonists and somatostatin, with patterns similar to those obtained for the secretory inhibition. There was a significant correlation between the somatostatin release and the acid and pepsin secretion during infusion of the secretory inhibitors but not in the control state. This study shows that beta-adrenergic agonists have inhibitory effects on gastric secretion in vivo similar to those of somatostatin. Both somatostatin and the beta-adrenergic agonists stimulated the release of somatostatin from the gastric mucosa. beta-Adrenergic antagonists were without effects. Somatostatin thereby fulfils the requirements for an endogenous mediator of the beta-adrenergic inhibition.
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PMID:Beta-adrenergic agonists inhibit gastric acid and pepsin secretion through somatostatin release in dogs. 287 15

The purpose of the present study was to evaluate the effect of somatostatin on gastric acid secretion and pepsin secretion in conscious dogs with gastric fistula. Infusion of histamine stimulated dose-dependently the acid secretion, whereas pepsin secretion was decreased by the high doses of histamine. Somatostatin inhibited dose-dependently the stimulated acid secretion but only with a maximum of 40%. The pepsin secretion was inhibited by somatostatin dose-dependently and with a higher potency. The acid inhibition was of a competitive type and prostaglandin-independent.
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PMID:Effect of somatostatin on histamine-stimulated gastric acid and pepsin secretion in dogs. 287 17

Somatostatin and somatostatin derivatives were tested for their ability to prevent gastric hemorrhagic erosions induced by ethanol. The somatostatin analogues were cyclohexapeptides with the rearranged amino acids 7-14 of somatostatin (S-14): Phe-Thr-Lys(Z)-Trp-Phe-D-Pro(I), Phe-Thr-Lys-Trp-Phe-D-Pro(II), Phe-Thr-Lys-D-Trp-Phe-Tyr(III) and Tyr-Phe-D-Trp-Lys-Thr-Phe(IV). In Spraque-Dawley rats receiving ethanol alone, the lesions involved 18.1 +/- 3.2% of the glandular stomach while after S- 14 (10(-7) mol/rat) the lesioned area was reduced to 6.3 +/- 1.1% (p less than 0.05). Peptide I and peptide II (doses 10(-7) -10(-9) mol/rat) decreased the area of erosions to less than 5%. Peptide III was less active and peptide IV was inactive. In rats with chronic gastric fistula S- 14 and peptide II decreased the cysteamine-stimulated acid secretion without affecting the pepsin output. We also continuously measured the intraluminal pH in the stomach of Wistar rats which develop gastric erosions after subcutaneous injection of cysteamine. The erosions were reduced by S- 14 or SMS while the intraluminal pH did not change under the influence of cysteamine or the combination of cysteamine plus S- 14 or SMS. Thus some of the peptides derived from S- 14 exert prominent gastric mucosal protection without influencing gastric secretion.
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PMID:Gastric mucosal protection by somatostatins. 288 58

To further investigate differences in the responses of normals and patients with duodenal ulcer with respect to gastrin release and acid and pepsin secretion, we infused bombesin (1 microgram/kg X h) or bethanechol (40 micrograms/kg X h) during the middle hour of a 3-h infusion of pentagastrin and compared the results with a pentagastrin infusion without added drug. Pentagastrin dosage (0.1 microgram/kg X h) was set to give about half-maximal response, to detect either inhibition or further stimulation of gastric secretion, whereas the dose of bombesin was chosen to give maximal gastrin but less than maximal acid secretion. Serum gastrin and somatostatin were also measured. In all subjects tested, bethanechol produced no effects on acid, gastrin, or somatostatin release but increased pepsin output. By contrast, bombesin inhibited pentagastrin-stimulated acid output in all 6 normal men by an average of 55%, whereas it inhibited acid output in only 2 of the 9 men with duodenal ulcer. Serum gastrin increases after bombesin in duodenal ulcer were three to four times greater than in normals. Although bombesin stimulates acid only by releasing gastrin, we postulate that bombesin may also simultaneously limit acid and pepsin secretion and speculate that this effect could be mediated by bombesin-induced somatostatin release. The cause for differences between duodenal ulcer and normal remain speculative.
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PMID:Divergent effects of bombesin and bethanechol on stimulated gastric secretion in duodenal ulcer and in normal men. 288 66

A humoral mechanism, potentiating the maximal acid, but not the pepsin response to exogenous gastrin in cats, is activated by protein-rich food in the stomach or duodenum, but not in the jejunum. In the present study, the effect of an oral meat meal on the maximal acid response to pentagastrin was investigated in Heidenhain pouch (HP) cats, and in antrectomized HP cats with duodenal exclusion and gastrojejunostomy Rouxen-Y. Antrectomy and duodenal exclusion abolished the postprandial HP acid response, and feeding did not potentiate the acid response to pentagastrin. The finding suggests that the gastrin-potentiating mechanism in the stomach is localized in the antrum, and it cannot be demonstrated in the jejunum. The basal plasma levels of gastrin and somatostatin did not differ in antrectomized and non-antrectomized cats. Antrectomy and duodenal exclusion abolished the postprandial gastrin and somatostatin responses. The plasma somatostatin increase during pentagastrin infusion persisted after antrectomy and duodenal exclusion. It is concluded that the antrum is not mandatory for the basal plasma levels of gastrin and somatostatin, but the postprandial gastrin response is of antral origin and may release somatostatin. Pentagastrin infusion releases extra-antral somatostatin in cats.
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PMID:Antrum participates in the postprandial augmentation of the acid response to exogenous gastrin in conscious cats. 288 10

The effects of a cow's milk diet on receptor activity and histamine metabolism in gastric glands and mucosa isolated from adult rats were examined. The milk diet was associated with (1) a decreased mobilization of H2 receptors by histamine and (2) an increased mobilization of PGE2 (prostaglandin E2) receptors in mucous cells (cytoprotective effect) and parietal cells (antiacid effect). These changes are not observed for the receptors reducing pentagastrin- and histamine-induced gastric acid secretion (pancreatic/enteroglucagons, somatostatin) and stimulating mucus, bicarbonate and pepsin secretions in the rat (secretin). Cimetidine produced a parallel displacement of the histamine dose-response curve, suggesting competitive inhibition between this classical H2 receptor antagonist and histamine in the two experimental groups. Prostaglandins and other components in milk such as EGF (epidermal growth factor) and somatostatin might therefore protect gastric mucosa by a differential control of PGE2 and histamine H2 receptor activity either directly (PGE2 in milk) or indirectly (inhibition of endogenous histamine synthesis/release and stimulation of PGE-I synthesis/release).
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PMID:Up- and down-regulation of membrane receptors as possible mechanisms related to the antiulcer actions of milk in rat gastric mucosa. 288 97

Somatostatin is located predominantly in D-cells of the antral and fundic area of the stomach and in the duodenal bulb. Furthermore, somatostatin is contained in neurons of the extrinsic and intrinsic nervous system. Somatostatin inhibits gastric acid, pepsin and gastrin secretion, and it stimulates gastric mucous secretion. All in all, somatostatin could exert protection of the gastric mucosa by reduction of aggressive and augmentation of protective mechanisms. There is, however, no evidence for a role of somatostatin in the pathogenesis of peptic ulcer. Endogenous opioids which have to be considered as potential peptidergic neurotransmitters increase vagal and postprandial gastric acid secretion and accordingly cannot be considered as a protective factor. Vasoactive intestinal peptide (VIP), also a peptidergic neurotransmitter, reduces acid and stimulates mucous and bicarbonate secretion. If this is of physiological relevance remains to be established. Secretin might be a protective factor for the gastric mucosa by stimulating mucous and bicarbonate secretion. On the other hand, it augments pepsin secretion which might attenuate any potential protective effects of secretin.
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PMID:[Somatostatin and opioids, secretin and VIP--protectors of the mucosa?]. 288


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