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

The aim of the present investigation was to study how bombesin, gastrin-17, cholecystokinin-8 (CCK-8) and electrical vagal stimulation influence the release of gastrin and somatostatin into the gastric lumen. Bombesin (3 and 30 nmol kg-1 h-1), gastrin-17 and CCK-8 (10 nmol kg-1h-1) were infused i.v. and vagal stimulations at 5 V, 2 ms, 5 Hz were performed in anaesthetized rats, in which the stomach was perfused with a dextran solution (pH approximately 6 or approximately 1.5). pH, gastrin and somatostatin levels were measured in the perfusate after having passed the stomach. In addition, blood samples were drawn from the jugular vein in the experiments in which bombesin was infused. Gastrin and somatostatin levels were determined with radioimmunoassay, and gastrin- and somatostatin-like immunoreactivity will be referred to as gastrin and somatostatin below. Infusion of bombesin, 3 and 30 nmol kg-1 h-1, did not influence acid secretion as evidenced by an unchanged intraluminal pH. Nor was the intraluminal secretion of gastrin or somatostatin influenced by bombesin, whereas plasma gastrin and somatostatin levels were significantly increased at the higher dose. In contrast, infusion of CCK-8 and gastrin-17 (10 nmol kg-1 h-1), as well as electrical vagal stimulation, significantly decreased the pH and increased the somatostatin levels in the perfusate. Vagal activation in addition increased the gastrin levels. The present results, demonstrating that bombesin influences plasma and perfusate levels of gastrin and somatostatin differently, indicate that intraluminal and intravascular gastrin and somatostatin release may be separately regulated.
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PMID:Differential effect of bombesin on intraluminal and intravascular release of gastric gastrin and somatostatin in anaesthetized rats. 256 66

Regulatory effects of insulin, somatostatin and cholecystokinin on amino acid transport in the isolated perfused rat pancreas have been studied using a rapid dual isotope dilution technique. Uni-directional L-serine transport (15 s) was quantified relative to an extracellular tracer D-mannitol over a wide range of substrate concentrations. In pancreata perfused with 2.5 mmol/l D-glucose, a weighted nonlinear regression analysis of overall transport indicated an apparent Km = 14.4 +/- 1.6 mmol/l and Vmax = 25.9 +/- 1.4 mumol.min-1.g-1 (n = 6). Although L-serine transport was stimulated during perfusion with 100 microU/ml bovine insulin, endogenous insulin (7-25 ng.min-1.g-1) released during continuous perfusion with either 8.8 mmol/l or 16.8 mmol/l D-glucose had no such effect. Exogenous somatostatin-14 (250 pg/ml) or cholecystokinin octapeptide (CCK-8, 3 x 10(-11) mol/l) appeared to increase only the Km for transport. Only CCK-8 evoked a notable protein output (2.9 +/- 0.3 mg.30 min-1.g-1) and juice flow (68 +/- 10 microliters.30 min-1.g-1, n = 3) from the exocrine pancreas. When pancreata were perfused with bovine insulin (100 microU/ml) and somatostatin-14 (250 pg/ml), the stimulatory action of exogenous insulin on L-serine transport was abolished. If endogenous insulin and somatostatin, released concurrently in response to 16.8 mmol/l D-glucose, were conveyed to the exocrine epithelium via an islet-acinar portal axis, it is conceivable that somatostatin modulates the stimulatory action of insulin on basolateral amino acid transport in the exocrine pancreas.
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PMID:Paradoxical effects of endogenous and exogenous insulin on amino acid transport activity in the isolated rat pancreas: somatostatin-14 inhibits insulin action. 256 59

The morphology and function islets isolated from rat pancreases with short-term (16 days) exocrine atrophy was investigated. It was found that this type of atrophy induced changes in the shape and morphological structure of pancreatic islets. However, the function of isolate islets did not change, as investigated by the basal or glucose-stimulated secretion of insulin, glucagon and somatostatin, and by the CCK-stimulated secretion of insulin. We conclude that the rat pancreas brought to atrophy by a short-term ligation of the pancreatic duct can be considered as a rich source of functionally viable islets.
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PMID:Pancreatic islets obtained from pancreases with short-term exocrine atrophy disturbed morphology but normal in vitro response to various stimuli. 257 Jul 8

Species differences have been observed in the effect of cholecystokinin octapeptide (CCK OP) on the canine and guinea pig gallbladder smooth muscle motility. 1. CCK OP was more potent stimulant in canine than in guinea pig gallbladder smooth muscles. Its pD2 values were 10 and 9.2, respectively. 2. The acetylcholine (10(-4) M)-induced maximum contractions in canine gallbladder muscle strips were by 50% lower as compared to the CCK OP (10(-8) M) maximum responses while in guinea pig gallbladder muscle strips the acetylcholine (ACh) maximum responses were by 20% lower than the CCK OP maximum responses. 3. CCK OP increased [3H]ACh release by 27% in canine gallbladder and by 40% in guinea pig gallbladder. 4. Somatostatin (SOM) had not any direct myogenic effect in guinea pig and canine gallbladder but it decreased [3H]ACh release from gallbladder intrinsic cholinergic neurons.
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PMID:Effect of cholecystokinin octapeptide and somatostatin on the motility of guinea pig and canine gallbladder. 257 94

The distribution and time of appearance of cells with gastrin/CCK-, neurotensin- and somatostatin-like immunoreactivity were studied in samples from eight regions of the gastrointestinal tract of chick embryos from 11 days of incubation to hatching. No immunoreactive cells were found in any region at 11 days of incubation. Somatostatin- and neurotensin-immunoreactive cells appeared for the first time in the proventriculus, pyloric region and duodenum at 12 days of incubation with cells immunoreactive for neurotensin occurring in the rectum at the same stage. Gastrin/CCK-immunoreactive cells were detected in the small intestine first at 14 days and in the pyloric region two days later. Cells immunoreactive for somatostatin and neurotensin appeared in the upper and lower ileum at 14 days of incubation for the first time; neurotensin-immunoreactive cells, present in the caecum at 14 and 16 days, were rare. Cells of all three types were plentiful in the pyloric region by 17 1/2 days of incubation. No immunoreactive cells were detected in the gizzard at any stage studied. Endocrine cells were present in the relatively undifferentiated surface epithelium which occurs throughout the gastrointestinal tract of chick embryos at 12 days of incubation. Thereafter cells of all three types were detected in the glandular epithelium at or very soon after morphogenesis and differentiation of the latter had occurred.
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PMID:The distribution and ontogeny of gastrin/CCK-, somatostatin- and neurotensin-immunoreactive cells in the gastrointestinal tract of the chicken. 257 89

The effects of an intravenous infusion of cholecystokinin octapeptide (CCK-8, 1 microgram.kg-1.h-1) were investigated in conscious fasted dogs chronically fitted with strain-gauge transducers on the antrum, the jejunum, and the colon. Attempts to antagonize the increase of motility appearing at the three levels during CCK infusion were made using different blockers to elucidate the mechanisms involved. Asperlicin (a specific CCK antagonist) blocked the effects of CCK-8 at the three levels, while atropine and somatostatin were only effective in the jejunum and colon. Methyl-levallorphan (a mu-opiate antagonist that poorly crosses the blood-brain barrier) antagonized the CCK-induced colonic stimulation when intracerebroventricularly administered. Serotonin, histamine, substance P, and K-antagonists as well as a benzodiazepine did not modify the CCK-8 induced stimulation. It was concluded that the stimulatory effect of CCK-8 resulted from (a) a direct stimulation of the smooth muscle cells at gastric level, (b) a cholinergic activation of the jejunum and the colon, and (c) the involvement of a mu-opioid central component in the colonic response only.
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PMID:Involvement of different mechanisms in the stimulatory effects of cholecystokinin octapeptide on gastrointestinal and colonic motility in dogs. 261 18

Pancreastatin is a 49-amino acid straight chain molecule isolated from porcine pancreatic extracts. In the perfused rat pancreas, this peptide has been shown to inhibit unstimulated insulin release and the insulin responses to glucose, arginine, and tolbutamide. To further explore the influence of pancreastatin on islet cell secretion, the effect of synthetic porcine pancreastatin (a 2-micrograms priming dose, followed by constant infusion at a concentration of 15.7 nmol/L) was studied on the insulin, glucagon, and somatostatin responses to 1 nmol/L vasoactive intestinal peptide (VIP), 1 nmol/L gastric inhibitory peptide (GIP), and 1 nmol/L 26 to 33 octapeptide form of cholecystokinin (8-CCK). The effect of pancreastatin on the insulin and somatostatin secretion elicited by glucagon (20 nmol/L) was also examined. Pancreastatin infusion consistently reduced the insulin responses to VIP, GIP, and 8-CCK without modifying glucagon or somatostatin release. It also inhibited the insulin release but not the somatostatin output induced by glucagon. These observations broaden the spectrum of pancreastatin as an inhibitor of insulin release. The finding that pancreastatin does not alter glucagon or somatostatin secretion supports the concept that it influences the B cell directly, and not through an A cell or D cell paracrine effect.
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PMID:Pancreastatin inhibits insulin secretion as induced by glucagon, vasoactive intestinal peptide, gastric inhibitory peptide, and 8-cholecystokinin in the perfused rat pancreas. 266 67

1. Preliminary, general chemical characteristics of substances in artificial sea water (ASW) washed through stimulated body wall (SBW) and in hemolymph taken from noxiously stimulated animals (SHL) were consistent with those of classical neurotransmitters, amino acids, and small- to medium-sized peptides. 2. 5-Hydroxytryptamine (5HT) and acetylcholine (ACh), unlike SBW and SHL, caused relaxation when perfused into isolated body wall. FMRFamide produced a biphasic response--brief contraction followed by prolonged relaxation. 3. Small cardioactive peptide (SCPB) caused body wall contractions similar to those produced by SBW and SHL, except that SCPB contractions displayed more desensitization and were completely blocked by 30 mM CoCl2. SCPB and SBW contractions were synergistic. 4. Dopamine caused persistent body wall contractions similar to those of SBW and SHL. Dopamine contractions were reduced but not blocked by 30 mM CoCl2. Unlike SBW activity, dopamine activity was reduced by alkalinization. 5. Glutamate and taurine produced strong but usually short-lasting body wall contractions. Adenosine, octopamine, arginine vasotocin, and cholecystokinin (CCK-8) caused weak or variable contractions. Met-enkephalin and somatostatin caused no obvious body wall responses. 6. When superfused over the fully sheathed abdominal ganglion, FMRFamide, met-enkephalin, glutamate, aspartate, and taurine reduced the magnitude of the gill-withdrawal reflex elicited by siphon nerve stimulation. 7. Taken together with earlier results, these data suggest a preliminary framework for trauma signal pathways. It is proposed that stress hormones (perhaps including FMRFamide, SCPs, 5HT, and dopamine) are released into hemolymph from neuroendocrine cells. Effective amounts of active intracellular solutes such as amino acids may also be released by extensive cellular rupture. Various humoral signals produce slow effects that contribute to hemostasis, balling up, increased cardiac output, and reflex suppression.
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PMID:Humoral factors released during trauma of Aplysia body wall. II. Effects of possible mediators. 276 Feb 88

The impact of overnight intravenous lipid emulsion (ILE) infusion on upper gastrointestinal tract physiology was assessed in 10 healthy volunteers. No changes in lower esophageal sphincter pressure (before infusion: 28 +/- 4 mm Hg; after infusion 20.5 +/- 3; p:NS), plasma concentrations of gastrointestinal hormones (gastrin: preprandial before/after lipids: 14 +/- 2.1/13 +/- 1.4 pM; postprandial before/after lipids: 28 +/- 2.7/30 +/- 3.4 pM, CCK: preprandial before/after lipids: 69 +/- 10/64 +/- 10 pM; postprandial before/after lipids: 96 +/- 11/95 +/- 12 pM; neurotensin: levels less than 6 pM in all samples; somatostatin levels undetectable in all samples) nor on pathologic gastroesophageal reflux episodes (% of time of pH less than 4, before/after lipids: 0.6 +/- 0.4/0.15 +/- 0.09), were found (p = NS). In contrast, technetium gastric emptying studies showed a significant delay when comparing pre- and post-lipid infusion values (37 +/- 4/54 +/- 4%) (p greater than 0.005). The mechanism of this effect remains unexplained.
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PMID:Intravenous fat emulsion (intralipid) delays gastric emptying, but does not cause gastroesophageal reflux in healthy volunteers. 276 Oct 66

Radioimmunoassays of brain extracts have shown that several peptides occur in high concentrations in the CNS. The releasing-factor peptides TRF, LRF, somatostatin, CRF and GRF have the highest concentration in the hypothalamic extracts. High levels of somatostatin, CCK octapeptide, neuropeptide Y (NPY) and vasoactive intestinal peptide (VIP) are found in cortical extracts. Substance P, CCK, NPY, and enkephalins are present in high concentrations in basal ganglia and mesolimbic areas. Pharmacological doses of these peptides result in several behavioural and vegetative effects. Immunocytochemical studies show that the CNS peptides are localised in neurones and in synaptic vesicles. In vitro studies with brain tissues show that peptides are capable of modifying the ongoing classical neurotransmission. In depressive patients several neuropeptides (CCK, CRF and NPY) have been shown to have low CSF levels. Patients dying of senile dementia have low cortical levels of somatostatin, CRF and substance P. In schizophrenic patients CCK peptides have shown to improve some symptoms. At present the therapeutic potentials of peptides are poorly known. More studies are required to understand their role in neurotransmission and related pathological states.
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PMID:Peptides and neurotransmission in the central nervous system. 282 29


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