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 graded doses of bethanechol on pancreatic secretion and plasma levels of pancreatic polypeptide and somatostatin was investigated in six healthy volunteers. In other studies the effect of a bethanechol background on the secretin-CCK stimulation of pancreatic secretion was also studied. Bethanechol caused a moderate stimulation of amylase secretion with a weak stimulation of bicarbonate secretion. These effects were not associated with significant changes in the plasma level of pancreatic polypeptide and somatostatin. Bethanechol enhanced the response to secretin and CCK. These results confirm a cholinergic pathway in the stimulation of pancreatic secretion in man.
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PMID:Cholinergic stimulation of human pancreatic secretion. 287 22

The effects of somatostatin (SOM) and cholecystokinin octapeptide (CCK-8) on basal and potassium-evoked release of neurotransmitter amino acids were investigated in slices of rat caudate nucleus (CN) and, for comparison, cerebral cortex (CX). Endogenous aspartate (Asp), glutamate (Glu), glycine (Gly), and gamma-aminobutyric acid (GABA) were measured by high performance liquid chromatography. In both CN and CX, potassium (5-55 mM) produced a concentration-dependent increase in the release of Asp, Glu, Gly, and GABA in the presence of extracellular Ca2+. CCK-8 (1 microM) stimulated in CN the basal and K+-evoked release of Gly to 231% and 160% of control, respectively; this effect was blocked by sulpiride (SULP), a dopamine receptor antagonist. In contrast, SOM (1 microM) inhibited the K+-evoked release of Glu in CN by 26%, an effect that was not blocked by SULP. SOM and CCK-8 did not significantly affect the basal or K+ (35 mM)-evoked release of other amino acids in the CN or of any amino acids in CX. The results indicate that: CCK-8 facilitation of Gly release is dependent of Gly release is dependent on dopamine receptor activation, whereas the inhibition by SOM of Glu release is not: and the effects of SOM and CCK-8 are specific with respect to the brain region affected.
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PMID:Somatostatin and CCK-8 modulate release of striatal amino acids: role of dopamine receptors. 287 62

The effects of somatostatin (SOM) and cholecystokinin octapeptide (CCK-8) on basal and potassium-induced release of acetylcholine (ACh) were investigated in slices of rat caudate nucleus (CN) and, for comparison, cerebral cortex (CX). Potassium (5-55 mM) produced a concentration-dependent increase in the release of [3H]ACh in the presence of extracellular Ca2+. SOM (1 microM), CCK-8 (1 microM) and the dopamine (DA) receptor agonist, apomorphine (APO, 30 microM) inhibited the K+-induced (35 mM) release of [3H]ACh by 26-32% from CN, but did not affect ACh release from CX. Other peptides (1 microM), such as Met-enkephalin, vasoactive intestinal peptide, thyrotropin-releasing hormone and substance P, had no effect on release of [3H]ACh in CN or CX. Sulpiride (SULP), a dopamine receptor antagonist, prevented the effects of APO and SOM, but not CCK-8, to inhibit [3H]ACh release. The results indicate that: (1) SOM and CCK-8 inhibit the release of [3H]ACh in CN, but not CX; and (2) the inhibitory effect of SOM, but not CCK-8, on [3H]ACh release is mediated by dopaminergic mechanisms.
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PMID:Somatostatin and cholecystokinin octapeptide differentially modulate the release of [3H]acetylcholine from caudate nucleus but not cerebral cortex: role of dopamine receptor activation. 287 39

A large number of antisera mainly raised against mammalian hormones are tested immunocytochemically on the GEP-endocrine system of mouse and fish (Barbus conchonius). The endocrine pancreas of mouse and fish appeared to contain the same four endocrine cell types; insulin-, glucagon-, PP- and somatostatin-immunoreactive cells. In mouse about 13 GEP endocrine cell types are distinguished: 1. insulin-, 2. somatostatin-, 3. glucagon-, 4. PP-, 5. (entero)glucagon-/PP-like, 6. CCK-like, 7. substance P-, 8. neurotensin-, 9. VIP-, 10. gastrin-, 11. secretin-, 12. beta-endorphin-, 13. serotonin-immunoreactive cells. Based on this and a previous study at least 13 GEP endocrine cell types seems to be present in stomachless fish: 1-9 as described for mouse, 10. (entero)glucagon-like, 11. met-enkephalin, 12. VIP-like, 13. unspecific immunoreactive endocrine cells. Coexistence of glucagon and PP-like peptides is found in the gut and pancreas of mice and in the gut of B. conchonius. In mouse pancreas and fish gut, endocrine cells showing only PP- or glucagon-like immunoreactivity are found too. In mouse stomach some endocrine cells showing only PP-immunoreactivity are demonstrated. In the same region coexistence of C-t-gastrin- and FMRF-amide-immunoreactivity is found in endocrine cells. The importance of these phenomena are discussed. Enteric nerves immunoreactive with antisera raised against substance P and GRP are found in mouse, against somatostatin and met-enkephalin in both mouse and fish and against VIP in fish.
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PMID:Immunocytochemical identification and localization of peptide hormones in the gastro-entero-pancreatic (GEP) endocrine system of the mouse and a stomachless fish, Barbus conchonius. 287 13

The effects of somatostatin on pancreatic secretion were studied in conscious rats during diversion and recirculation of pancreatic juice. Pancreatic secretion was significantly inhibited by low doses (2 micrograms/kg/h) of somatostatin during diversion of pancreatic juice. The inhibitory effect was more marked on bicarbonate and protein output than on volume, while in bicarbonate and protein output a rebound effect was observed. These data suggest a combined inhibitory effect of somatostatin on endogenous CCK release and cholinergic mechanisms. During recirculation of pancreatic juice there was no rebound effect, thus only the inhibition of cholinergic mechanisms seems to be involved in the inhibitory effect of somatostatin. During recirculation, CCK-OP-stimulated bicarbonate and protein secretion was strongly inhibited by somatostatin. Even water secretion not stimulated by CCK-OP was significantly inhibited demonstrating a supplementary inhibitory effect on basal cholinergic mechanisms. Somatostatin decreased only slightly the synthetic secretin-stimulated water and bicarbonate secretion. The more effective inhibition of protein output was explained by an additive effect of somatostatin on basal cholinergic tone.
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PMID:Effects of somatostatin on basal and stimulated pancreatic secretion in conscious rat. 287 34

We measured the ability of CCK-8 alone, a test meal alone, or a combination of the two, to increase peripheral plasma somatostatin levels in the baboon. Baboons received a five-minute intravenous infusion of either CCK-8 (1, 2, or 4 micrograms/kg) or saline prior to a 30-minute meal. CCK-8 administration at all doses resulted in a significant rise of plasma somatostatin-like immunoreactivity (SLI). In addition, ingestion of a meal following a control saline infusion resulted in a significant rise of plasma SLI. However, the meal-related rise in SLI was blunted by prior administration of CCK-8 at all doses, including a dose which did not significantly decrease meal size. CCK-8 administration at all doses also blunted the meal-related rise of plasma insulin and glucose. We conclude that the known ability of CCK-8 to inhibit gastric emptying, as well as to decrease meal size, may account for its suppression of the meal-related SLI release.
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PMID:Effect of CCK-8 on basal and meal-stimulated somatostatin in the baboon. 287 77

Cellular mechanisms underlying the actions of antisecretory agents were studied with dispersed canine fundic cells; aminopyrine accumulation monitored parietal cell (PC) function. Canine PC have pharmacologically typical histamine (H) H2 and muscarinic (M) receptors. PC also have gastrin (G) receptors, which were selectively blocked by gastrin/CCK antagonists. Potentiating interactions occurred between secretagogues, one of the components of the interdependency between regulatory pathways. Prostaglandins (PG) E2 inhibited H-stimulated PC function. Treatment of PC with pertussis toxin (PT), which inactivates the inhibitory GTP-binding protein of adenylate cyclase (Gi), markedly reduced PG inhibition, indicating PG action via Gi. PC function can also be directly inhibited by H+/K+-ATPase inhibitors, such as omeprazole. When canine mucosal cells were studied, stimulatory G and inhibitory M receptors were present on fundic somatostatin (S) cells. Histamine was localized to canine fundic mast cells, which lacked G or M receptors, a conclusion that may not pertain to fundic histamine cells in other species. Nonparietal cell receptors may be important modulators of the regulation of acid secretion.
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PMID:Mechanisms of action of antisecretory drugs. Studies on isolated canine fundic mucosal cells. 288 44

We determined the effects of exogenous somatostatin-14 (100 and 200 ng/kg/h; mimicking postprandial somatostatin concentrations) on pancreatic responses to a background infusion of secretion in combination with graded doses of CCK-8 in conscious dogs with chronic gastric and duodenal fistulas. The lower dose of somatostatin-14 (S-14), which produced S-14 plasma levels lower than measured after a meal, did not change basal or stimulated pancreatic secretion. The upper dose of S-14, which produced plasma S-14 concentrations slightly above the postprandial range, caused inhibition of pancreatic fluid and protein secretion to low doses of CCK-8 (p less than 0.05). The inhibition was surmountable with higher doses of CCK-8. We interpret these data as indicating that circulating S-14 is not an important hormonal regulator of exocrine pancreatic secretion.
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PMID:Effect of circulating somatostatin on exocrine pancreatic secretion in conscious dogs. 288 2

Calcitonin gene-related peptide (CGRP) exists in nerves throughout the gastrointestinal tract and pancreas, and exogenous CGRP has been reported to inhibit many endocrine and exocrine secretions of the gut and pancreas. Because somatostatin also has widespread inhibitory actions and because both gut and pancreatic somatostatin secretion may be under peptidergic control, we examined the influence of CGRP on circulating levels of somatostatin-like immunoreactivity (SLI) and on hormone output from the duodenal lobe of the dog pancreas in situ. Intravenous infusion of human CGRP in anesthetized dogs increased arterial SLI in a dose-dependent manner. During iv infusion of CGRP at 500 pmol/min, the increment of circulating SLI (change at 20 min, +175 +/- 24 fmol/ml) was composed of nearly equimolar amounts of SLI-14 and SLI-28, suggesting an effect of CGRP on both gastric and intestinal somatostatin secretion. The effect of iv CGRP (500 pmol/min) on arterial SLI exceeded those of iv CCK-8 (440 pmol/min), iv isoproterenol (10 nmol/min), and intragastric administration of acidified liver extract. In contrast, salmon calcitonin (500 pmol/min, iv) was without effect. CGRP did not stimulate pancreatic SLI output when infused iv (500 pmol/min) or when infused directly into a pancreatic artery (5 pmol/min). The pancreatic infusion of CGRP decreased insulin output slightly (change at 20 min, -21 +/- 8%), but did not affect glucagon output. We conclude that CGRP is a most effective yet selective stimulator of gastrointestinal somatostatin release, with little influence on islet function. We suggest that exogenous and possibly endogenous neuronal CGRP could exert inhibitory effects on gastrointestinal function via the release of somatostatin.
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PMID:Calcitonin gene-related peptide: a potent and selective stimulator of gastrointestinal somatostatin secretion. 288 97

The gastro-entero-pancreatic (GEP) endocrine system of a stomach-containing and of a stomachless teleost, Sparus auratus and Barbus conchonius, respectively, are studied immunocytochemically using different antisera against mammalian hormones. Insulin-, glucagon-, somatostatin-, and pancreatic polypeptide (PP)-immunoreactive cells are identified in the endocrine pancreas of both species. Only the distribution of PP-immunoreactive cells differed strongly; in the principal islet of both fishes, few PP-immunoreactive cells are present, whereas in the smaller ones many of them are observed in S. auratus and none in B. conchonius. In the digestive tract of S. auratus 10 endocrine cell types can be distinguished: neurotensin-, secretin-, serotonin-, somatostatin-, and two types of substance P-immunoreactive cells exclusively in the stomach, and C-t-gastrin/CCK-, glucagon-, Met-enkephalin-, PP-, and only one type of substance P-immunoreactive cells in the intestinal epithelium. With the exception of substance P-immunoreactive cells, the other four intestinal endocrine cells, as well as an unspecific immunoreactive cell, can also be found in B. conchonius. Coexistence of glucagon- and PP-like immunoreactivity is observed in the pancreas of S. auratus and in the gut of B. conchonius. Pancreatic and gut endocrine cells showing only PP- or glucagon-like immunoreactivity are found, too.
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PMID:A comparative immunocytochemical study of the gastro-entero-pancreatic (GEP) endocrine system in a stomachless and a stomach-containing teleost. 288 63


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