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)

Six normal humans each underwent infusions of 1) saline; 2) propranolol; 3) somatostatin; 4) somatostatin with propranolol; and 5) somatostatin with propranolol plus phentolamine on separate occasions. Propranolol alone had no effect on glucose production or plasma glucose. Somatostatin alone produced the expected initial decrease followed by an increase in both hepatic glucose production and plasma glucose. beta-Adrenergic blockade with propranolol displaced the glucose production (MANOVA, P = 0.0220) and plasma glucose (MANOVA, P = 0.0057) somatostatin response curves to higher levels, whereas alpha-adrenergic blockade with phentolamine combined with beta-adrenergic blockade displaced the glucose production (MANOVA, P = 0.0281) and plasma glucose (MANOVA, P = 0.0134) somatostatin response curves to lower levels. Because plasma insulin, C-peptide, and glucagon were suppressed comparably under all three conditions and plasma glucose concentrations were comparable initially, this represents direct alpha-adrenergic stimulation of hepatic glucose production in postabsorptive humans demonstrable when the primary glucoregulatory hormones are withdrawn and beta-adrenergic mechanisms are blocked. It is best attributed to sympathetic neural norepinephrine release.
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PMID:Direct alpha-adrenergic stimulation of hepatic glucose production in human subjects. 614 Aug 54

The effect of adrenergic agonists and antagonists on the secretion of gastric somatostatin-like immunoreactivity (SLI) and gastrin was investigated in an isolated, vascularly perfused rat stomach preparation. Two- to six-fold increases in SLI secretion induced by isoproterenol, epinephrine, and norepinephrine were completely abolished by propranolol but were not influenced by phentolamine. Propranolol did not alter glucagon- and DB-cAMP-induced stimulation of SLI release. Experiments in which the beta 2-agonist salbutamol and the beta 1- and beta 2-blockers practolol and H35/25 were used showed that both subtypes of beta receptors are involved. Gastrin secretion revealed only minor changes in dose-response studies with a wide range of isoproterenol concentrations (2 X 10(-8) to 1.5 X 10(-4) M). The results obtained in this study suggest that in rats 1) the SLI response to adrenergic agonism is predominantly mediated by beta receptors; 2) both beta 1- and beta 2-adrenergic receptors are involved; 3) under in vitro conditions, adrenergic agonism is a weak stimulus for gastrin secretion.
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PMID:Adrenergic control of rat gastric somatostatin and gastrin release. 614 72

This study had a dual purpose. First, the effects of pancreatic buffer flow on whole organ hormone output were investigated. Second, the receptor mechanisms by which sympathetic nerve stimulation alters the secretion rates of somatostatin and insulin were assessed. Pancreata of mongrel puppies were perfused in situ with nonrecirculated Krebs-Ringer bicarbonate buffer (150 mg/dl glucose). Buffer flow was adjusted between 0.2 and 4 ml/min X g pancreas. Insulin secretion rate (nanograms per min/g pancreas; ISR) as well as pancreatic O2 and glucose consumption increased as flow increased between 1 and 2 ml/min X g, where each reached a maximum plateau. Thus, ISR was shown to be dependent on flow over the middle range of flow investigated. In separate experiments, bilateral stimulation of the splanchnic nerves or pancreatic arterial infusion of norepinephrine to a final concentration of 60 microM decreased ISR and the somatostatin secretion rate (SSR). Adrenergic suppression of ISR was antagonized by phentolamine and phenoxybenzamine. Adrenergic inhibition of SSR was blocked only by phenoxybenzamine. Propranolol had no effects. We conclude that norepinephrine is sufficient to account for sympathetic inhibition of ISR and SSR (e.g. it is not necessary to postulate another transmitter) and that this inhibition may be transmitted through an effect on the islet vasculature or an effect on the islet cells themselves. The types of alpha-adrenoceptors mediating the adrenergically induced decrease in ISR differ from those causing the decrease in SSR.
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PMID:Neural control of pancreatic insulin and somatostatin secretion. 614 13

The response of insulinoma tissue to glucose, alpha-ketoisocaproate, and the modifiers of insulin release, tolbutamide, isoproterenol, and acetylcholine, was studied. Tumor tissue was transplanted under the kidney capsule of 14 rats, and the tumor-bearing kidneys were perfused in vitro about 8 weeks later. The plasma glucose concentration of these animals was 85.0 +/- 7.0 mg/dl, while the plasma insulin concentration was 13.8 +/- 1.5 ng/ml (normal, 180.5 +/- 7.0 mg/dl and 2.6 +/- 0.5 ng/ml, respectively; n = 26). Glucose (30 mM) evoked a 3- to 5-fold increase in insulin secretion, similar to the increase seen when either 100 micrograms/ml tolbutamide or 0.5 micrograms/ml isoproterenol were added to the perfusion medium containing 5 mM glucose. Propranolol at 50 micrograms/ml, but not at 20 micrograms/ml, inhibited insulin release stimulated by isoproterenol. Acetylcholine (10 or 100 microM) did not stimulate insulin secretion. alpha-Ketoisocaproate caused the highest insulin release of all stimuli studied. Glucagon or somatostatin release was not seen in any of the experiments. These results show that the tumor tissue transplanted under the kidney capsule responds not only to model fuels, but also to the sulfonylurea class of drugs and to adrenergic agents.
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PMID:Pharmacological modifications of insulin release in vitro from fuel-responsive transplantable insulinomas. 614 33

Drug therapy for acute variceal bleeding should be viewed as an adjunct to emergency sclerotherapy. Its role in preventing very early rebleeding (within days) following sclerotherapy needs to be established. The best candidates for such a role are somatostatin and octreotide, but glypressin and vasopressin and nitroglycerin combinations have therapeutic effects in the short-term. Propranolol is the drug for long-term prevention of rebleeding and prevention of the first variceal bleed. For primary prophylaxis it significantly reduces the rate of bleeding, and there is a trend towards reducing mortality. It should be used in cirrhotic patients with large varices. For secondary prophylaxis, propranolol significantly reduces rebleeding but does not improve survival. The reduction in rebleeding is similar to long-term sclerotherapy when compared in randomized studies. There is no value in adding beta-blockers to sclerotherapy compared with sclerotherapy alone, but few studies have evaluated the effects after the eradication of varices. beta-Blockers can be used as the first-line therapy to prevent variceal rebleeding. They also have been shown to reduce the frequency of rebleeding from congestive gastropathy. Many patients do not have a portal pressure reduction with propranolol. The addition of isosorbide mononitrate converts many nonresponders to responders. Current clinical trials are evaluating if therapeutic efficacy is improved by these drug combinations.
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PMID:Pharmacological therapy for portal hypertension: rationale and results. 755 72

After bilateral superior cervical ganglionectomy (SCGx) of adult male rats, norepinephrine (NE) content of the medial basal hypothalamus (MBH) decreased significantly by 39-47% from 16 h to 7 days after surgery. During this time the levels of serum growth hormone (GH) and prolactin (PRL) and of MBH GH-releasing hormone (GRH), thyrotropin-releasing hormone (TRH) and somatostatin were measured by RIA. In sham-operated controls, serum PRL increased and serum GH decreased 16-24 h after surgery, attaining pre-surgical levels later on. In SCGx rats, significantly lower serum GH and PRL and higher MBH GRH and TRH content as compared to controls was observed 16-24 h after surgery, during the wallerian degeneration phase after SCGx. MBH somatostatin concentration decreased in SCGx rats 20 h after surgery. Two injections of the alpha 1-adrenoceptor blocker prazosin 45 and 90 min before sacrifice, alone or together with the beta-blocker propranolol, prevented the changes in MBH hypophysiotropic hormone content, as well as in serum GH and PRL levels, found in SCGx rats 20 h after surgery. Propranolol treatment did not affect hormone levels. Neither drug modified the decrease in MBH NE content observed after SCGx. The results argue in favor of the existence of physiologically relevant projections from superior cervical ganglion neurons to the MBH controlling hypophysiotropic hormone release.
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PMID:Changes in serum growth hormone and prolactin levels, and in hypothalamic growth hormone-releasing hormone, thyrotropin-releasing hormone and somatostatin content, after superior cervical sympathectomy in rats. 790 22

DL-Propranolol (PRO), a beta-adrenergic blocking agent, and the neuropeptide somatostatin (SS) have central nervous system depressant and anticonvulsive properties. To investigate a possible relationship between these two components, we studied the influence of PRO and DL-isoproterenol (ISO), a beta-adrenergic agonist, on the somatostatinergic system in the rat frontoparietal cortex. The short- (5 h) and long-term (14 days) administration of ISO (5 mg/kg, intraperitoneally (i.p.)), or of PRO (10 mg/kg, i.p.) did not affect somatostatin-like immunoreactivity (SLI) content in the frontoparietal cortex of male Wistar rats. Both short- and long-term ISO administration decreased the number of specific [125I]Tyr11-SS receptors in synaptosomes from frontoparietal cortex (31%, P < 0.05, and 26%, P < 0.02, after short- and long-term administration, respectively) without changing the affinity constant. This decrease in the number of [125I]Tyr11-SS receptors was not due to a direct effect of ISO on these receptors since no decrease in binding was produced by high concentrations of ISO (10(-5) M) when added in vitro. This decrease could be blocked by pretreatment with PRO. Short- and long-term administration of PRO alone produced an increase in the [125I]Tyr11-SS binding in frontoparietal cortex (26%, P < 0.02, and 40%, P < 0.001, after short- or long-term administration, respectively) without changing the affinity constant.
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PMID:Modulation by isoproterenol and propranolol of somatostatin receptors in synaptosomes from rat frontoparietal cortex. 810 12

The effects of catecholamines (CATS) infused into the hepatic portal vein were studied in ten 18-h-fasted conscious dogs. Glucose production (GP) and gluconeogenesis (GNG) were assessed using tracer ([3H]glucose, [14C]alanine) and arteriovenous difference techniques. Each experiment consisted of a 100-min equilibration, a 40-min basal, and two 90-min test periods. A pancreatic clamp (somatostatin + basal portal insulin and glucagon) was used to fix insulin and glucagon at basal levels. Propranolol (1 microgram.kg-1.min-1) and phentolamine (2 micrograms.kg-1.min-1) were infused intraportally during both test periods of the blockade group while a carrier solution was infused in the control group. Norepinephrine (NE; 100 ng.kg-1.min-1) and epinephrine (Epi; 40 ng.kg-1.min-1) were infused intraportally during the second test period of both protocols. Portal NE (70 +/- 46 to 8,404 +/- 674 and 162 +/- 57 to 6,530 +/- 624 pg/ml, respectively) and portal Epi (21 +/- 11 to 3,587 +/- 309 and 29 +/- 6 to 2,989 +/- 406 pg/ml, respectively) rose in the control and adrenergic blockade groups, respectively. The increases in arterial NE and Epi were modest in both groups. Intraportal infusion of CATS increased GP from 2.1 +/- 0.2 to 6.2 +/- 1.0 mg.kg-1.min-1 in the control group but did not change it (2.7 +/- 0.4 to 2.7 +/- 0.3 mg.kg-1.min-1) in the blockade group. Portal CATS had no effect on GNG in the presence or absence of adrenergic blockade (GNG rose from 0.7 +/- 0.2 to 0.9 +/- 0.2 and 0.8 +/- 0.2 to 1.0 +/- 0.2 mg.kg-1.min-1 in the control and blockade groups, respectively). In conclusion, portal infusion of catecholamines significantly augmented GP by selectively stimulating glycogenolysis. The increase in hepatic GP could be completely inhibited by intraportal adrenergic blockade.
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PMID:Direct effects of catecholamines on hepatic glucose production in conscious dog are due to glycogenolysis. 876 90

Although somatostatin (somatotrophin release inhibitory factor; SRIF) is a well-known inhibitory peptide, there are only a few reports of it acting as a positive modulator. In this work, the action of somatostatin upon rat submandibular protein secretion was studied. In vivo somatostatin infusion (35 microg/(kg h)) raised protein secretion stimulated by adrenergic and peptidergic agents. To rule out possible systemic effects of somatostatin, in vitro experiments were performed. Somatostatin (90 nmol/l) augmented protein release stimulated by noradrenaline (19 micromol/l) and substance P (10 micromol/l), but it did not affect isoprenaline (400 micromol/l)-induced protein release. Phenoxybenzamine (20 micromol/l) reduced the effect of somatostatin on noradrenaline-stimulated protein release. Propranolol (20 micromol/l) increased the noradrenaline-stimulated protein release and this effect was synergistic with the action of somatostatin. The absence of extracellular calcium did not significantly reduce somatostatin enhancement of agonist-induced secretion. Fluorescence measurements of the Ca(2+)-sensitive dye fluo3 showed that cytosolic calcium in acinar cells remained elevated during stimuli when somatostatin was present in the medium. It was concluded that somatostatin modulates rat submandibular protein secretion by prolonging the time that the cytosolic calcium signal remains high after stimulus.
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PMID:Modulation by somatostatin of rat submandibular salivary secretion. 1264 58

Gastric hemangiomas are rare benign vascular tumors that can cause severe gastrointestinal system bleeding. We presented the case of a neonate with fresh bleeding and melena from the orogastric tube and detected gastric hemangioma in esophagogastroduodenoscopic examination. Propranolol is widely used in treatment of cutaneous hemangiomas and non-gastric gastrointestinal system hemangiomas. However, the surgical approach is preferred for treating gastric hemangiomas, and there are few reports of gastric hemangiomas associated with non-surgical treatment. Gastric hemorrhage decreased with antacid and somatostatin treatment. Propranolol treatment was initiated before the surgery decision. After three weeks of treatment, we observed regression in the hemangioma with endoscopic evaluation. During the course of treatment, the patient's gastrointestinal system bleeding did not recur, and there were no side effects associated with propranolol.
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PMID:A Newborn with Gastric Hemangioma Treated Using Propranolol. 3034 49


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