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)

We have examined the actions of vasoactive intestinal peptide (VIP) and certain other known immune modulators on a nuclear pool(s) of protein kinase C (PKC) in isolated rat splenocyte nuclei. Rat splenocyte nuclei pure by enzymatic and electron microscope criteria demonstrated a time- and concentration-dependent activation of nuclear PKC (nPKC) by VIP. A biphasic pattern of three bell-shaped curves was observed with peak phosphorylation at 10(-15), 10(-9) and 10(-6)M VIP. The phosphorylation of endogenous nuclear substrates was characterized as a PKC-mediated event by use of three known PKC inhibitors, 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7), sphingosine, and staurosporine, which produced similar phosphate incorporation measurements. Also, this activity was blocked with the addition of a monoclonal antibody to PKC. Inhibitors of the ability of VIP to activate nPKC included somatostatin, 8-bromo-cAMP, peripheral benzodiazepine receptor modulators, and the PKC inhibitors, sphingosine and staurosporine. These data have direct relevance to our knowledge of cell-mediated immunity.
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PMID:Vasoactive intestinal peptide (VIP) activation of nuclear protein kinase C in purified nuclei of rat splenocytes. 197 36

The effect of massive small bowel resection on the immunostaining of neuropeptides in the submucous plexus of the retained small intestine was examined. The neuropeptides chosen were somatostatin and vasoactive intestinal polypeptide because these are markers for two of the major populations of neurons in the plexus. Three different methods were used to assess the effect of resection on the enteric nervous system. Firstly immunocytochemical staining of neuropeptide containing neurons and nerve fibers was compared between test and control animals. The results demonstrated a significant increase in the number and size of the vasoactive intestinal polypeptide containing neurons with no change in the number of somatostatin neurons although these were also increased in size. Secondly the possibility that the increase in neuron number might be the result of neuronal division was examined by 3H-thymidine incorporation experiments. The results demonstrated that no neuronal elements were labelled. Finally the possibility that the increase in vasoactive intestinal peptide was the result of an increase in transcription was assessed by Northern blot analysis. The results demonstrated a small but significant increase in mRNA levels. It was concluded that massive small bowel resection directly affects neuropeptide levels in the submucous plexus, resulting in an increase in vasoactive intestinal polypeptide-immunoreactive neurons.
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PMID:Effect of massive small bowel resection on components of the peptidergic innervation of the rat small intestine. 197 76

In 41 patients, operated upon for common bile duct stones, a temporary bile fistula was achieved by means of a T-tube and a Foley-catheter with an occludable balloon. To learn more about peptide control of bile secretion, 6-8 days after surgery, bile flow was studied before as well as during infusion of the three peptides somatostatin, vasoactive intestinal peptide and secretin. The findings, also presented in Figure 17, were: 1. During somatostatin infusion, bile secretion decreased by 30%, and bile lipid output was reduced by some 10%. The clearance of [14C]-erythritol decreased by 25%, indicating an effect on the bile acid-dependent canalicular bile secretion (Paper I). 2. Vasoactive intestinal peptide (VIP) increased bile secretion by 65%. The concentration of bile lipids decreased, whereas the output was uneffected. The bicarbonate concentration increased, and the concentrations of sodium and potassium were uneffected. [14C]-erythritol clearance was not influenced by VIP infusion. Thus, VIP stimulated bile secretion at the ductular level (Paper II). 3. VIP increased bile secretion by 60%, whereupon secretin increased it by another 70%. Neither of the two peptides effected bile acid output. Both VIP and secretin increased bicarbonate output, whereas only VIP increased the concentration. The clearance of [14C]-erythritol was uneffected by VIP infusion, but increased following secretin, as did the clearance of [14C]-mannitol. Thus, VIP stimulated bile secretion at the ductular level, whereas secretin seemed to stimulate bile secretion both at the ductular level and at the bile acid non-dependent canalicular level (Paper III). 4. Whereas VIP stimulated bile secretion, somatostatin decreased it by some 40%. Even when somatostatin was administered during VIP infusion, no reduction of the VIP-induced choleresis was seen. VIP increased both bicarbonate concentration and output, whereas somatostatin had the opposite effect. The concentration of chloride increased following VIP infusion, but decreased following somatostatin. The output of bile acids was not influenced by VIP infusion and decreased by somatostatin, whereas total lipid concentration increased during somatostatin infusion with a decrease when VIP was added. Thus, somatostatin acts on the bile acid-dependent canalicular bile secretion and also, to some extent, on the ductular secretion. The effects of the two peptides on bile secretion are independent of each other (Paper IV). 5. While fasting, 6-8 days after bile duct surgery, bile secretion averaged 290 microliters/min. Canalicular bile secretion, as measured by the clearance of [14C]-erythritol, constituted some 80% of total bile flow. Maximum de novo synthesis of bile acids was 8.7 mmol/24 h, implying a 8-9 fold stimulation due to interrupted enterohepatic circulation (Paper V). 6. No serious side effects from this method with temporary bile fistulas following bile duct surgery were found. Therefore, the method is recommended for further research on human bile secretion (Paper V).
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PMID:Bile secretion in man. The effects of somatostatin, vasoactive intestinal peptide and secretin. 198 35

The effect of vasoactive intestinal peptide (VIP) on the release of growth hormone (GH) from the adenohypophysis of the goat was studied in vitro using the perifusion system. Two perifusion systems were employed to differentiate potential direct effects of VIP on the pituitary from indirect effects mediated through the hypothalamus. The first perifusion system used single chambers housing only pituitary fragments. The second system used two chambers in tandem, one containing hypothalamus and the second the pituitary fragments, the flow passing through the hypothalamic chamber first. VIP (10(-6), 10(-7), 10(-8)M) stimulated significant GH release in both perifusion systems (P less than 0.05, P less than 0.01) in a concentration related fashion. The quantity of GH release induced by the 10(-9)M and 10(-10)M VIP groups were not significant. Further, the GH released from the system that perifused the pituitary alone (10(-8)M VIP) was significantly higher than that containing both the hypothalamus and the pituitary fragments (P less than 0.05). The relative lower GH secretory response to the same dose of VIP applied to the hypothalamus-pituitary suggests that the perifused caprine hypothalamus may release an inhibitory factor, such as somatostatin in vitro. These results suggest that VIP stimulates GH release by acting directly on the adenohypophysis of the goat.
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PMID:Effect of vasoactive intestinal peptide on the release of growth hormone in perifused pituitary and hypothalamus of the goat. 201 23

To facilitate analysis of the regulation of epithelial Cl- transport by hormones, neurotransmitters, and autocrine mediators, we have developed a primary monolayer culture system for shark rectal gland (SRG) epithelial cells. Cultures exhibit vigorous transcellular Cl- secretion which can be measured using short-circuit current or 36Cl flux methods. Transport is markedly reduced by bumetanide or barium, inhibitors of Na(+)-K(+)-2Cl- cotransport and K+ channels, respectively. This indicates that Cl- secretion by SRG monolayers occurs by a mechanism similar to that described in numerous native Cl- secretory epithelia. Forskolin, 10 microM 2-chloroadenosine, or vasoactive intestinal peptide, potent secretagogues in the isolated perfused SRG, stimulate Cl- secretion by SRG cultures. Submicromolar concentrations of 2-chloroadenosine, which inhibit Cl- secretion in the native SRG, reduce forskolin-stimulated short-circuit current in SRG cultures. Somatostatin, another inhibitor of Cl- secretion by the native SRG, reduces forskolin-stimulated adenosine 3',5'-cyclic monophosphate accumulation in SRG cultures. These results demonstrate that SRG cultures are fully responsive to mediators which activate or inhibit secretion by the native epithelium.
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PMID:Cl- secretion by cultured shark rectal gland cells. I. Transepithelial transport. 201 13

The effect of intrathecal (i.t.) vasoactive intestinal peptide (VIP) and an analogue of growth hormone releasing factor (GRF) with putative VIP antagonistic property, (Ac-Try1, D-Phe2)-GRF-(1-29), on the nociceptive flexor reflex was studied in decerebrate, spinalized, unanesthetized rats. VIP (10 pM) facilitated the flexor reflex for several minutes. A similar facilitation was induced by the VIP antagonist applied i.t. with a potency 15 times less than that of VIP. Pre-administration of the VIP antagonist dose-dependently antagonized the reflex facilitation by i.t. VIP. In contrast, the reflex facilitation induced by i.t. substance P, somatostatin, calcitonin gene-related peptide and galanin was not influenced by the VIP-antagonist. The VIP antagonist by itself did not depress the flexor reflex over the dose range of 3 pM-3 nM and neither did it block the facilitation of the flexor reflex induced by a brief conditioning electrical stimulus train that activated the C-afferents in skin innervated by the sural nerve. The present results indicate that this GRF analogue is an effective and specific VIP antagonist in the rat spinal cord. Furthermore, it is suggested that VIP may not be involved in the transmission of cutaneous nociceptive information under normal conditions.
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PMID:An analogue of growth hormone releasing factor (GRF), (Ac-Try1, D-Phe2)-GRF-(1-29), specifically antagonizes the facilitation of the flexor reflex induced by intrathecal vasoactive intestinal peptide in rat spinal cord. 206 98

In this study, we characterize the glucagon receptors on rat retinal particulate preparations. The specific binding of 125I-glucagon was saturable and reversible. Apparent equilibrium conditions were established within 30-45 min. Analysis of binding data is compatible with the existence of two classes of binding sites: a high-affinity class with a KD of 7 +/- 0.8 nM and a Bmax of 2.3 +/- 0.2 pmol/mg of protein and a low-affinity class with a KD of 84.4 +/- 2.5 nM and a Bmax of 16.5 +/- 2.3 pmol/mg of protein. The 125I-glucagon binding to retinal particulate preparation was not inhibited by 1 microM concentrations of insulin, atrial natriuretic factor, angiotensin II, somatostatin, and vasoactive intestinal peptide. However, synthetic human pancreatic growth hormone-releasing factor, hGRF-44, inhibited binding, although the concentration required for half-maximal displacement was 10-fold higher than that for native glucagon. Glucagon binding was GTP sensitive. Inclusion of 0.1 mM GTP in the binding assay produced an increase in the concentration of unlabeled glucagon required for half-maximal displacement of 125I-glucagon, from 23 to 220 nM. Glucagon stimulated adenylate cyclase formation in retinal particulate preparations. The concentration of glucagon required for half-maximal activation of retinal adenylate cyclase was 16.2 nM. These results suggest that glucagon may play a role as a neurosignal transmitter in rat retina.
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PMID:Identification of glucagon receptors in rat retina. 215 17

Interleukin-6 (IL-6) is an inflammatory cytokine that is produced by a variety of cells and tissues. We recently demonstrated that IL-6 is produced by anterior pituitary cells in response to the bacterial endotoxin lipopolysaccharide and phorbol diester in vitro. Lipopolysaccharide (0.01-100 ng/ml) increased, whereas dexamethasone (0.1-100 nM) decreased, IL-6 production by anterior pituitary cells in vitro as measured by the 7TD1 cell growth factor assay. In addition, we now report that IL-6 production by anterior pituitary cells is stimulated by agents that elevate intracellular cAMP concentrations. Exposure of anterior pituitary cells to (Bu)2cAMP (0.01-10 mM), prostaglandin E2 (1.0-1000 nM), forskolin (50-1000 nM), or cholera toxin (0.25-250 ng/ml) for 6 h resulted in concentration-related increases in the production of IL-6, which, in the cases of forskolin and cholera toxin, correlated well with increased intracellular cAMP concentrations. Vasoactive intestinal peptide (1-1000 nM), which stimulates adenylate cyclase activity in the anterior pituitary, caused a concentration-related enhancement of IL-6 production that was unaffected in the presence of 10-100 nM somatostatin. In contrast, GH-releasing factor had no effect on IL-6 production. These data suggest that anterior pituitary cells produce IL-6 in response to increased intracellular cAMP, and that the neuropeptide vasoactive intestinal peptide may act to regulate IL-6 production.
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PMID:Production of interleukin-6 by anterior pituitary cells is stimulated by increased intracellular adenosine 3',5'-monophosphate and vasoactive intestinal peptide. 216 22

Preincubation of HT29 cells with an alpha-2 adrenergic agonist resulted in a parallel rightward shift in the subsequent dose-response curve to 5-bromo-6-[2-imidazoline-2-yl-amino] quinoxaline (an alpha-2 adrenergic agonist) in inhibiting vasoactive intestinal peptide-stimulated cyclic AMP production. This rightward shift in the dose-response curve, which was concentration and time dependent, was interpreted as desensitization of the alpha-2 adrenergic receptor-mediated inhibition of cyclic AMP production. The fact that no decrease in efficacy was observed appears to result from a receptor reserve. Agonist preincubation effects on subsequent p-aminoclonidine (an alpha-2 adrenergic partial agonist) inhibition and partial irreversible inactivation of receptors confirmed the presence of an alpha-2 adrenergic receptor reserve in HT29 cells. Desensitization appeared to have a heterologous component since inhibition of vasoactive intestinal peptide-stimulated cyclic AMP production by somatostatin was also attenuated. We also assessed the effect of alpha-2 agonist preincubation on subsequent 5-bromo-6-[2-imidazoline-2-yl-amino] quinoxaline inhibition of parathyroid hormone-stimulated cyclic AMP production in OK cells. As with HT29 cells, agonist preincubation resulted in a concentration- and time-dependent shift in the dose-response curve. In both cell lines, long-term preincubation with an alpha-2 adrenergic agonist resulted in a 40% decrease in subsequent [3H]yohimbine binding, indicating down-regulation of the alpha-2 adrenergic receptor.
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PMID:Desensitization of the alpha-2 adrenergic receptor in HT29 and opossum kidney cell lines. 216 96

We report the case of a VIPoma diagnosed in a 15-year-old teenager who experienced profuse secretory diarrhea associated with hypokalemia, metabolic acidosis and high plasma levels of vasoactive intestinal peptide (VIP) and pancreatic polypeptide (PP). Angiography showed an abnormal mass in the head of the pancreas. Before surgery, subcutaneous injections (100 micrograms every 8 hours) of the long-acting somatostatin analogue octreotide or SMS 201-995, were administered in order to stabilize the clinical status of the patient and to reduce the intravenous administration of fluid and electrolytes. This treatment resulted in prompt relief of the symptoms and in a partial decrease of the plasma levels of VIP and PP. At subsequent laparotomy, there was a tumour localized in the head of the pancreas, which was completely removed by Whipple resection. The immunohistochemical staining revealed the presence of VIP and PP inside the tumour cells. Two years after surgical resection, the patient is healthy without clinical or laboratory evidence of recurrence.
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PMID:[Vipoma in an adolescent: treatment with a delayed-action somatostatin analog, octreotide or SMS 201-995, and surgical removal]. 217 28


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