Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Propranolol, a beta adrenergic blocking drug, is known to inhibit the thyrotropin (TSH) stimulation of adenosine-3',5'-monophosphate (cyclic AMP production in thyroid membranes but the mechansim of this inhibitory action is known. We have therefore investigated the influence of propranolol on the binding of 125I-labelled TSH to human thyroid membranes. Both d- and l-propranolol were found to enhance the binding of 125I-labelled TSH to thyroid membranes. The amount of label bound increased from about 30% in the absence of propranolol to about 60% in the presence of 3.3 x 10(-3)M propranolol. Scatchard analysis of the binding data indicated that propranolol increased the association constant of the thyrotropin-thyrotropin receptor interaction. Practolol, lithium carbonate, methimazole, and somatostatin had no effect on thyrotropin binding. This effect of propranolol appeared to be due to a direct reversible action of propranolol on the thyroid membranes and could be attributed to the membrane-disrupting properties of the drug rather than its beta-blocking activity. The increased TSH receptor occupancy which resulted from the increased association constant of the TSH-thyroid membrane interaction corresponded with a decrease in TSH-stimulated cyclic AMP formation. These data could indicate that propranolol reduced the efficiency of the receptor-adenylyl cyclase coupling system.
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PMID:The influence of propranolol on the thyrotropin receptor. 18 96

The aim of this study was to compare the metabolic and hormonal effects of somatostatin to those of propranolol, a beta-adrenergic blocking agent known to reduce basal insulin secretion. For this purpose, 6 normal subjects received somatostatin (4 microgram/min) per 60 min and 6 subjects were infused with propranolol (0.08 mg/min). Somatostatin resulted in a significant decrease of basal insulin (p less than 0.05) and glucagon (p less than 0.01) and raised plasma FFA levels from a mean basal value of 417 +/- 24 muEq/1 (x +/- SEM) to 600 +/- 46 muEq/1 at 60 min (p less than 0.01). Propranolol significantly decreased basal insulin (p less than 0.05) and glucagon (p less than 0.05); FFA levels rose slightly at the end of propranolol administration (p less than 0.05). The levels of FFA which were significantly higher (p less than 0.025) during somatostatin as compared to those observed during propranolol, seem to suggest a role for this tetradecapeptide in lipid metabolism independent of its inhibiting action on islet hormone release.
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PMID:A comparative study of metabolic and hormonal responses to somatostatin and propranolol in man. 45 22

1) Emergency treatment. The best treatment remains endoscopic sclerotherapy, which controls the bleeding in 90% of the cases. Pharmacologic management stops the variceal hemorrhage in 80% of the cases and is indicated before endoscopic treatment can be performed. Intravenous somatostatin administration may be prolonged for 5 days, even more, and may thus prevent early rebleeding, which is not achieved neither by vasopressin nor by glypressin, which administration is restricted to 24 hours. Esophageal tamponade is useful to arrest a massive variceal bleeding, if vasoactive drugs are not available or not efficient, before endoscopic management. If the bleeding persists after 2 sclerotherapy sessions, an alternative treatment is mandatory: the patient should be sent to the surgeon for a portosystemic shunt if the operative risk is acceptable (child A and B) or should become a candidate for a transjugular intrahepatic stent shunt, especially if transplantation is considered afterwards. 2) Prevention of recurrent hemorrhage. A) Early (within 5 days after the initial bleeding). Somatostatin probably prevents early rebleeding, as do sclerotherapy. B) Late. B blockade (+ nitrates) or long-term sclerotherapy have the same efficacy. Their association may improve their results. 3) Prevention of the first bleeding episode. Propranolol decrease the risk of variceal rupture from 20% to 9% during the first year after the diagnosis of esophageal varices and is the only treatment which may be proposed to cirrhotics who did not yet bled form their varices.
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PMID:[Prevention and treatment of digestive hemorrhage due to ruptured esophageal varices in patients with cirrhosis]. 136 Oct 90

A total of 112 3-week old Wistar rats were separated into eight groups: control groups I-IV (n = 62) and propranolol-treated groups V-VIII (n = 50). Propranolol hydrochloride (100 mg/kg) was present in the rats' drinking water until 26 weeks of age and growth rates of all groups were monitored daily until 53 days of age and thereafter every third day throughout the study. Chronic oral propranolol administration produced growth retardation (P less than 0.05) in both sexes that was reversible when treatment was discontinued. Organ weights were generally smaller in propranolol-treated rats; on the other hand, the ratio of most organ weights per 100 g of body weight was greater in propranolol-treated rats (especially females). The radio-immunological determination of plasma growth hormone showed increased concentrations of growth hormone in propranolol-treated rats (P less than 0.05), whereas hypothalamic somatostatin content was not significantly changed. The results showed that the retarded growth rate following chronic oral propranolol administration to growing rats was independent of changes in plasma growth hormone and hypothalamic somatostatin concentrations, and that retardation was entirely reversible when the beta-adrenoceptor antagonist was discontinued.
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PMID:Mechanism of growth retardation following chronic administration of beta-adrenoceptor antagonists to developing rats. 168 Jul 61

GH-releasing peptide (GHRP; His-D-Trp-Ala-Trp-D-Phe-Lys-NH2), a hexapeptide derived from enkephalin, has been shown to have GH-releasing activity in man and several animal species. To characterize the GHRP dose-response curve and compare it with that of GH-releasing hormone [GHRH-(1-44)NH2], six unanesthetized young adult cynomolgus macaques were tested with a range of iv doses of GHRP or GHRH in random order. Animals were fitted with vests and tethers. Blood samples were obtained before and at 15-min intervals after the administration of drugs. Doses ranged from 0.03-3 mg/kg for GHRP and from 1-30 micrograms/kg for GHRH. The dose-response curves for the two peptides were not parallel. GHRP had lower potency, but evoked a much higher peak GH response than GHRH (greater than 55 vs. 12 micrograms/L). Because one of the proposed mechanisms of action of GHRP is the inhibition of somatostatin (SS), we tested the effects of propranolol, which inhibits SS, on the GH responses to GHRH and GHRP. Propranolol was given at a dose of 14 micrograms/kg, iv, 10 min before the injection of saline, GHRH (10 micrograms/kg), or GHRP (1 mg/kg). GH responses to propranolol alone did not differ from those to placebo (peak, 6 +/- 2 vs. 8 +/- 2 micrograms/L). However, propranolol pretreatment doubled the GH responses to both GHRH and GHRP compared with those to GHRH or GHRP alone 28 +/- 5 micrograms/L vs. 14 +/- 5 (P less than 0.05) and 54 +/- 2 vs. 25 +/- 6 micrograms/L (P less than 0.001), respectively]. These results show that GHRP causes a potent dose-dependent release of GH in this primate species. Since GHRP can produce a greater maximal GH response than GHRH, mechanisms other than release of endogenous GHRH must be involved.
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PMID:Growth hormone (GH) responses to the hexapeptide GH-releasing peptide and GH-releasing hormone (GHRH) in the cynomolgus macaque: evidence for non-GHRH-mediated responses. 185 62

A number of in vivo studies suggest that hypothalamic somatostatin (SRIF) tone is stimulated by the beta-adrenergic system. Employing dispersed adult male rat hypothalamic cells, we studied the effects of beta-adrenergic antagonists on the release of hypothalamic SRIF. Propranolol, at concentrations of 1-100 microM, had no detectable effect on basal SRIF release, but caused dose-dependent inhibition of SRIF release stimulated by ouabain. Two other beta-adrenergic antagonists, labetolol and metoprolol, also caused inhibition of ouabain-stimulated SRIF release. The alpha 2-agonist clonidine was without effect on SRIF release under basal or stimulated conditions. GH secretion from monolayers of dispersed rat anterior pituitary cells was also examined. Propranolol (1-100 microM) had no significant effect on basal GH secretion or GH secretion stimulated by rat GRF. In conclusion, 1) beta-adrenergic antagonists caused inhibition of stimulated SRIF release; 2) clonidine had no detectable effect on SRIF release; and 3) propranolol did not affect GH secretion in vitro. These findings support the hypothesis that beta-adrenergic antagonists augment GH responsivity by inhibiting hypothalamic SRIF release.
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PMID:Inhibition of hypothalamic somatostatin release by beta-adrenergic antagonists. 196 76

The effect of epinephrine on amino acid (AA) metabolism was examined in 33 healthy volunteers who participated in four studies. Nine subjects participated in study I, which consisted of four parts: euglycemic insulin clamp, insulin plus epinephrine, insulin plus epinephrine plus propranolol, and insulin plus propranolol. In study II six subjects received epinephrine with hepatic-femoral venous catheterization. In study III five individuals received epinephrine with somatostatin plus basal insulin replacement. In study IV quadriceps muscle biopsy was performed in six subjects after epinephrine or insulin infusion. Both epinephrine and insulin caused a generalized decline in all plasma AA except alanine. With combined epinephrine-insulin infusion, the decrease in plasma AA was additive. Propranolol blocked the hypoaminoacidemic effect of epinephrine but failed to alter the AA lowering action of insulin. Epinephrine, while maintaining basal insulinemia, reduced the catechol's hypoaminoacidemic effect by 39%. After epinephrine, splanchnic alanine uptake increased, but plasma alanine remained constant because of a parallel rise in muscle alanine production. Plasma/intracellular concentrations of branched-chain amino acids (BCAA) and all gluconeogenic amino acids, except alanine, decreased after both epinephrine and insulin. In summary, the effect of epinephrine on plasma/intracellular total, gluconeogenic, and BCAA concentrations is similar to insulin.
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PMID:Regulation of amino acid metabolism by epinephrine. 197 Jul 11

To determine whether GH feedback affects both induced and spontaneous GH secretion and to explore its neurotransmitter mediation, we assessed the effects of 6-h GH infusions (0.55-5.5 micrograms/m2/min) on sleep-associated and GH-releasing hormone (GHRH)-, insulin hypoglycemia-, and arginine-stimulated GH secretion and their modulation by beta-adrenergic blockade in normal men. GH infusions initiated 2 h before the expected onset of sleep produced a dose-dependent inhibition of GH secretion. GH infusions (0.55 micrograms/m2/min) initiated 4 h before the stimuli inhibited the GH response to each, but did not alter the TSH response to TRH. Propranolol infusion (80 micrograms/min) started 2 h before the onset of sleep or the stimulus enhanced GH responses to GHRH and insulin alone and in the presence of GH. In contrast, propranolol neither enhanced the GH responses to arginine or sleep nor reversed the inhibitory effects of GH. The negative feedback effect of GH to both physiological and pharmacological stimuli of GH secretion indicates that it is most likely mediated by both stimulation of somatostatin and inhibition of GHRH release. The effects of beta-adrenergic blockade suggest an inhibition of somatostatin release, although the complex interaction of GH and propranolol implies that they act through dissimilar mechanisms.
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PMID:Beta-adrenergic modulation of growth hormone (GH) autofeedback on sleep-associated and pharmacologically induced GH secretion. 257 14

Alpha adrenergic blockade with phentolamine (10 microM) reduces the glucagon response to severe glucopenia (from 150 to 25 mg/dl) to 22% of the control values in the isolated perfused rat pancreas. Propranolol (10 microM) had no significant effect. Neither alpha nor beta adrenergic blockade reduced the magnitude of glucopenic suppression of insulin secretion, but phentolamine increased insulin levels before and during glucopenia. The pattern of somatostatin secretion in these experiments resembled that of insulin. Depletion of norepinephrine from sympathetic nerve endings by pretreatment with 6-hydroxydopamine lowered the pancreatic norepinephrine content to less than 20% of control values and reduced the glucagon response to glucopenia to 69% of the controls. Combined alpha and beta adrenergic blockade during less severe glucopenia (from 120 to 60 mg/dl) reduced the glucagon response to 21% of controls. However, slight glucopenia (from 100 to 80 mg/dl), which elicited only 11% increase in glucagon in the control experiments, was not altered significantly by combined alpha and beta adrenergic blockade. Morphologic studies of adrenergic nerve terminals labeled with [3H]norepinephrine revealed associations with alpha cells. It is concluded that in the isolated rat pancreas adrenergic mediation accounts for most of the glucagon but not insulin response to glucopenia. It is controlled within the pancreas itself, possibly through a direct enhancement by glucopenia of norepinephrine release from nerve endings.
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PMID:Adrenergically mediated intrapancreatic control of the glucagon response to glucopenia in the isolated rat pancreas. 285 31

Drugs used to treat portal hypertension cause constriction of mesenteric arterioles, reducing inflow to the portal venous system, portal pressure, and flow through portasystemic collaterals (such as esophageal varices). Vasopressin and somatostatin are direct vasoconstrictors. Propranolol acts by blocking vasodilatory beta 1 receptors and reducing cardiac output. A major side effect of vasopressin therapy is impaired cardiac performance secondary to coronary vasoconstriction and increased work against high arterial pressure. Infusion of vasopressin together with a cardiac inotrope or a vasodilator, and administration of vasopressin as an inactive "hormonogen" which is slowly released in vivo, may lessen adverse effects. Somatostatin appears to act selectively in the mesenteric circulation. Controlled trials indicate that vasopressin may be useful for controlling hemorrhage from esophageal varices and that somatostatin works at least as well as vasopressin. Propranolol treatment has been used to prevent variceal bleeding; however, controlled trials of its effectiveness have produced conflicting results.
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PMID:Drug therapy for portal hypertension. 287 47


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