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)

Aside from studies of a possible synergism between T3 and glucocorticoids in regulating GH mRNA, there have been few previous studies of the modulation by hormones and other factors of glucocorticoid hormone regulation of pituitary cell GH gene expression. We have employed a serum-free medium containing no exogenously added Ca2+ to investigate whether Ca2+ or somatostatin influences the stimulation by the synthetic glucocorticoid dexamethasone of GH mRNA levels in GH3 cells. Basal levels were slightly (less than or equal to 2-fold) stimulated by CaCl2 (0.4 mM). The stimulation by dexamethasone (100 nM) of GH mRNA in GH3 cells incubated in serum-free medium with or without Ca2+ was, respectively, 20- and 25-fold. Thus, under these experimental conditions, little effect of Ca2+ on regulation by dexamethasone was observed. To further reduce Ca2+ levels in the incubation medium, EGTA (20 microM) was added to chelate residual Ca2+. In some but not all experiments, EGTA treatment yielded a slight decrease in basal GH mRNA levels. Time-course experiments performed in the presence of EGTA showed that during incubation periods with dexamethasone that yielded a detectable stimulation of GH mRNA (2-4 days), Ca2+ (0.4 mM) inhibited the dexamethasone stimulation by 3- to 5-fold. Investigations of the dose-response relationship of the effect of dexamethasone on GH mRNA performed under the same conditions showed that at dexamethasone concentrations that yielded a significant stimulation of GH mRNA (10 nM or greater), Ca2+ (0.4 mM) inhibited the dexamethasone stimulation by about 2-fold. In contrast to the inhibitory effects of Ca2+ on the stimulation by dexamethasone of GH mRNA in the GH3 cells, somatostatin had no effect at any concentration tested (1-1000 nM) on dexamethasone regulation of this mRNA.
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PMID:Glucocorticoid stimulation of growth hormone messenger ribonucleic acid levels in GH3 cells is inhibited by calcium but not by somatostatin. 288

Frog esophageal mucosa contains peptic glands which are innervated by cholinergic neurons. When incubated in a medium containing 1.5 mM CaCl2, pepsinogen release from esophageal mucosa was increased by a high potassium concentration (55 mM KCl), 1,1-dimethyl-4-phenylpiperazinium (DMPP) or bethanechol. Whereas the response to bethanechol remained little changed, the response to high KCl concentrations or DMPP was abolished in the absence of Ca2+. The stimulatory effects of high KCl concentrations and DMPP were also eliminated by the presence of atropine or somatostatin. Furthermore, pepsinogen release in response to bethanechol was dose-dependently inhibited by somatostatin. Frog esophagus was found to contain somatostatin-like immunoreactivity, with a higher density at the end adjacent to the stomach. Chromatography of mucosa extract on Sephadex G-50 revealed a single peak of somatostatin-like immunoreactivity that coeluted with somatostatin-14. Immunohistochemical staining of the mucosa with peroxidase antiperoxidase technique demonstrated the presence of two varieties of somatostatin-like immunoreactivity-containing cells, one individually dispersed within the intercalated septa and the other in groups within the interlobular septa of the peptic glands. These results seem to indicate that somatostatin or somatostatin-like immunoreactivity may play a modulatory role in neurally mediated pepsinogen secretion in the frog esophagus.
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PMID:Somatostatin modulation of neurally mediated pepsinogen secretion from frog esophageal mucosa. 289 27

Somatostatin in a hypothalamic peptide hormone which inhibits growth hormone release from the anterior pituitary. However, biochemical and morphological investigations have revealed that somatostatin is located not only in the hypothalamus but also in other brain areas (for example the cerebral cortex) where it occurs and in nerve cell bodies and fibres from which it can be released in a Ca2+-dependent manner. It has therefore been suggested that the neuropeptide may have functions in the central nervous system other than its effect on growth hormone release; one possible action is that of a neuromodulator. Therefore, hypothalamic and cerebral cortical slices of the rat were used to examine whether somatostatin modifies the electrically or CaCl2-evoked release of tritiated monoamines from monoaminergic neurones. it is reported here that somatostatin inhibits 3H-noradrenaline release from the hypothalamus (but not from the cerebral cortex) but does not affect the release of 3H-dopamine and 3H-serotonin.
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PMID:Somatostatin selectively inhibits noradrenaline release from hypothalamic neurones. 610 59

The present experiments were undertaken to investigate the effect of alteration in on extracellular calcium concentration and of somatostatin on cholecystokinin-(CCK)- and caerulein-induced insulin and glucagon release from the isolated perfused rat pancreas. In control studies using perfusate containing 2.5 mM CaCl2 and 50 mg/dl glucose, CCK and caerulein caused insulin and glucagon release in a dose-related fashion. During perfusion with calcium free medium, insulin release was markedly inhibited. Subsequent introduction of 2.5 mM CaCl2 to the medium restored insulin response toward control levels. Extracellular calcium depletion, however, had no effect on CCK- or caerulein-induced glucagon release. The output of glucagon in the absence of calcium was comparable to that seen in the control experiments. On the other hand, somatostatin abolished the increase in glucagon secretion, but not the increase in insulin secretion, when perfused simultaneously with CCK or caerulein. However, pretreatment for 10 min with somatostatin blocked even insulin secretion. However, pretreatment for 10 min with somatostatin blocked even insulin secretion. The effects of somatostatin on hormonal discharge are suggested to be related to an alteration in the handling of or response to calcium. Recently, somatostatin has also been shown to inhibit calcium uptake by islets. Thus, the present results indicate a differential sensitivity of CCK- and caerulein-stimulated alpha and beta cell to extracellular calcium depletion and to the effect of somatostatin.
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PMID:Effect of somatostatin and calcium deprivation on cholecystokinin or caerulein-induced insulin and glucagon release from the isolated perfused rat pancreas. 611 42

The effects of a five day treatment with calcium chloride (1 ml 0.11 M CaCl2/100g body weight i.p., twice daily) on somatostatin cells in gastric antral mucosa of white rats were investigated. Somatostatin cells of experimental and control animals were identified by immunoperoxidase method using rabbit antihuman antisomatostatin (1:1000), and counted on perpendicularly cut sections taken from four transversal levels going from pylorus to antrofundic border. The results obtained have demonstrated the occurrence of somatostatin cell hyperplasia in animals treated with calcium chloride, established on the ground of highly significant rise in the number of somatostatin cells and a change in their topography.
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PMID:The effect of five days calcium chloride treatment on the somatostatin cells of the antral mucosa in white rats. 614 59

Neurotensin-like immunoreactivity (NTLI) is released from the small intestine into the blood after enteral administration of fat and systemic administration of bombesin. The purpose of the present investigation in the rat was to study the effect of intravenously (i.v.) administered CaCl2 on the plasma concentration of NTLI (p-NTLI) and to investigate the effect of i.v. infusion of somatostatin on basal NTLI release, as well as that stimulated by fat, bombesin and CaCl2. Administration of CaCl2 (5-25 mg X kg-1) increased p-NTLI levels in a significant and dose-dependent manner. In contrast, somatostatin 25-200 ng X min-1) reduced the basal p-NTLI levels, as well as the increase in p-NTLI levels induced by CaCl2 (10 and 25 mg X kg-1), fat (oleic acid, 0.5 ml) and bombesin (25 and 125 pmol X kg-1), in a dose-related manner. Injection of bombesin released immunoreactive material that was indistinguishable from synthetic bovine neurotensin (1-13) upon gel-filtration. This material seemed to be rapidly converted to the more stable metabolite neurotensin (1-8).
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PMID:Increase in neurotensin-like immunoreactivity in rat plasma after administration of calcium, bombesin and fat and its inhibition by somatostatin. 615 37

We have prepared a fluorescent conjugate of porcine calmodulin with 5-(dimethylamino)-1-naphthalene-sulfonyl chloride that is highly sensitive to both calcium binding and protein binding. We have used the fluorescence of this conjugate in addition to the intrinsic peptide fluorescence to show that adrenocorticotropic hormone (ACTH), beta-endorphin, glucagon, and substance P undergo calcium-dependent binding by calmodulin, with competition for common binding sites. The dissociation constants determined in the presence of 0.85 mM CaCl2 and 0.2 N KC1, pH 7.3 at 25 degrees C, range from 1.5 muM to 3.4 muM. The alpha-melanocyte-stimulating hormone, bombesin, and somatostatin also bind, with dissociation constants between 60 muM and 90 muM. Angiotensins I and III, bradykinin, neurotensin, physalaemin, substance P octapeptide, insulin, and Leu- and Met-enkephalin show little or no binding. Sequence comparisons show that the peptides that bind calmodulin well contain regions structurally similar to the recognition sequence for the cAMP-dependent protein kinase and to the sequences surrounding phosphorylated serine residues in several calmodulin binding proteins. This result suggests that modification of calmodulin binding sites in calmodulin-dependent proteins is one of the functions of protein kinase. Calcium has a dual role in peptide binding by calmodulin. The occupation of calcium binding sites having a pK approximately 4 results in a 2-fold increase in peptide binding affinity.
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PMID:Binding of simple peptides, hormones, and neurotransmitters by calmodulin. 618 Jul 61

Somatostatin-14 elicits negative inotropic and chronotropic actions in atrial myocardium. Less is known about the effects of somatostatin-14 in ventricular myocardium. The direct contractile effects of somatostatin-14 were assessed using ventricular cardiomyocytes isolated from the hearts of adult rats. Cells were stimulated at 0.5 Hz with CaCl2 (2 mM) under basal conditions and in the presence of the beta-adrenoceptor agonist, isoprenaline (1 nM), or the selective inhibitor of the transient outward current (Ito), 4-aminopyridine (500 microM). Somatostatin-14 did not alter basal contractile response but it did inhibit (IC50 = 13 nM) the response to isoprenaline (1 nM). In the presence of 4-aminopyridine (500 microM), somatostatin-14 stimulated a positive contractile response (EC50 = 118 fM) that was attenuated markedly by diltiazem (100 nM). These data indicate that somatostatin-14 exerts dual effects directly in rat ventricular cardiomyocytes: (1) a negative contractile effect, observed in the presence of isoprenaline (1 nM), coupled to activation of Ito; and (2) a previously unreported and very potent positive contractile effect, unmasked by 4-aminopyridine (500 microM), coupled to the influx of calcium ions via L-type calcium channels. The greater potency of somatostatin-14 for producing the positive contractile effect indicates that the peptide may exert a predominantly stimulatory influence on the resting contractility of ventricular myocardium in vivo, whereas the negative contractile effect, observed at much higher concentrations, could indicate that localized elevations in the concentration of the peptide may serve as a negative regulatory influence to limit the detrimental effects of excessive stimulation of cardiomyocyte contractility.
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PMID:Positive and negative contractile effects of somatostatin-14 on rat ventricular cardiomyocytes. 1124 23

The aim of this study was to compare what changes are caused by high doses of cholecalciferol (100,000 UI vD3) and CaCl2 on thyroid parafollicular (C) cells and airways neuroendocrine (NE) cells in rat. Overdosage of vD3 and CaCl2 causes hypocalcaemia and strong hypercalcitoninemia in blood; C cells showed mainly signs of hypertrophy; simultaneously, the number of strong calcitoninpositive cells decreased significantly (statistically significant changes). Immunohistochemical reactions, detecting CGRP, somatostatin, synaptophysin and neuronspecific enolase did not fall under statistic analysis. Airways NE cells re-acted to hypercalcemia differently than C cells--they probably respond to different regulatory mechanisms.
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PMID:Estimation of influence of high doses of cholecalciferol on thyroid parafollicular and respiratory tract neuroendocrine cells; preliminary investigations. 1563 3