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)

The mechanism of action of adiphenine on in vitro rat anterior pituitary TSH release was compared to that of the physiological stimulator TRH. The comparative study showed that adiphenine and TRH were able to increase TSH release in a dose-dependent manner, had similar time courses of action for equipotent stimulating concentrations and produced similar aspects of stimulated TSH cells. However, there were several differences between the effects of adiphenine and TRH. Adiphenine action was inhibited by 20 mM K+; was not calcium dependent; was inhibited by neither thyroid hormones nor somatostatin; was little affected by energy depression. It is concluded that adiphenine probably acts near the ultimate steps of the TSH release pathway and could be a useful pharmacological tool for studying the mechanism of TSH release.
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PMID:Comparison of adiphenine and TRH effects on TSH release by rat pituitary in vitro. 1 85

1. Dibutyryl cyclic AMP (Db cAMP, 75-500 microgram/kg), injected into the lateral ventricle of the brain of the cat increased blood pressure, heart rate and splanchnic discharge rate. 2. ATP, but not AMP, induced similar changes; GMP in small doses increased blood pressure. 3. A number of drugs are known to activate adenylate cyclase-induced hypertension, tachycardia and increase splanchnic discharge rate. This was shown for TRH, tetracosactide and a new beta2-adrenoceptor stimulant, NAB 365. 4. Injection into the lateral ventricle of theophylline or Ro 7/2956, both inhibitors of phosphodiesterase, similarly increased blood pressure. 5. Histamine administered by the same route induced similar reactions; it is not known if this action was exerted by activation of H1- or H2-receptors. 6. Somatostatin, known to reduce cAMP levels, induced a small but significant decrease in blood pressure. Melanocyte stimulating hormone release inhibiting factor (MIF) and TSH were ineffective. 7. These results provide evidence for the possibility of a role for cAMP in the central regulation of blood pressure at suprabulbar levels.
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PMID:Cyclic 3'5'-adenosine monophosphate and central circulatory control in cats and dogs. 2 Feb 56

The effect of somatostatin on thyroid hormone secretion stimulated by TSH in man was studied. The injection of TSH into a thyroid artery during surgery was followed by an increase in the serum concentration of iodothyronines in the corresponding thyroid vein. This increase was significantly lower (p less than 0.02) when somatostatin was given as a bolus injection into a peripheral vein 5 min prior to the administration of TSH, and followed by a continuous infusion for 60 min. Since somatostatin-like immunoreactivity has been localized to some cells of the thyroid gland being in a parafollicular location, it is suggested that somatostatin may be an intrathyroidal regulator of thyroid activity in man.
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PMID:Somatostatin inhibits thyroid hormone secretion induced by exogenous TSH in man. 4 73

An iv administration of 1 ml sheep antiserum to somatostatin (anti-SS) resulted in marked increases of both serum GH and TSH, with a peak 10--20 min after administration in male rats anesthetized with urethane or pentobarbital. Administration of anti-SS had no effect on serum PRL. Ablation of the basal medial hypothalamus abolished the rises of both serum GH and TSH after anti-SS administration. Intravenous injection of 1 ml rabbit antiserum to TRH (anti-TRH) decreased serum TSH levels 15 min after injection, whereas injection of normal rabbit serum did not affect TSH levels. Serum TSH levels did not rise after injection of anti-SS in rats pretreated with anti-TRH. On the other hand, pretreatment with anti-TRH did not affect the basal serum GH levels nor the anti-SS-induced GH release. The enhanced secretion of GH and TSH after anti-SS injections was not blocked by pretreatment with indomethacin, an inhibitor of prostaglandin synthesis. The following conclusions were made: 1) both GH and TSH responses to anti-SS require an intact basal medial hypothalamus; (2) TSH response to anti-SS is mediated by hypothalamic TRH; and 3) the GH response may be mediated by hypothalamic GH-releasing hormone which is not TRH or prostaglandins.
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PMID:Studies on the mechanism of growth hormone and thyrotropin responses to somatostatin antiserum in anesthetized rats. 10 24

The endocrine glands of the human foetus are active early in gestation, and various foetal and placental hormonal contributions are essential for growth and sexual differentiation. 1. The anterior pituitary gland has the ability to synthesize, store and secrete hormones early in gestation. The patterns of change in plasma concentrations of hGH (Fig. 1), ACTH, LH and FSH (Fig. 2) during gestation indicate that secretion is at a maximum at mid-gestation, followed by a progressive decrease towards term. The high levels at mid-gestation can be interpreted as due simultaneously to a high secretion rate, low peripheral catabolism and absence of feedback mechanism. In contrast, the secretions of PRL (Fig. 1) and TSH are moderate at mid-gestation and only increase in the last trimester of gestation. 2. Effective control by the central nervous system (CNS) of the pituitary secretions is still immature at mid-gestation. The presence in the foetal hypothalamus of releasing factors such as LRF (Fig. 5) and TRF, and of somatostatin (Fig. 6), a growth hormone release inhibiting factor (GIF), has been established. TRF and GIF, but not LRF, are also present in the cerebral cortex. It has been postulated that, early in life, relatively autonomous and unrestrained secretion of hypothalamic hypophysiotropic releasing factors occurs, and that, later in development, there is a maturation of inhibitory or restraining influences mediated via the CNS (feedback mechanisms) that modulates the secretion of the foetal adenohypophyseal hormones (Fig. 3 and 4). 3. Observations made with anencephalic newborn confirm that a functional hypothalamus is necessary during foetal life for the secretion of each of the hormones of the anterior pituitary gland with the exception of PRL, the secretion of which is normal in anencephaly. Although somatostatin probably participates in the regulation of hGH during foetal life, it appears evident from the anencephaly data that this regulation can only be fully understood by postulating the existence of a growth hormone releasing factor (GRF).
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PMID:[Ontogenesis of hypothalamic control of adenohypophyseal secretions in the human foetus (author's transl)]. 11 47

The effects of synthetic linear somatostatin on basal circulating levels on several pituitary and pancreatic hormones, and of glucose and free fatty acids (FFA) were studied in 6 normal men after an overnight fast. A priming intravenous infusion of 250 mug of somatostatin in 18 sec was followed by a constant infusion of 500 mug over a period of 60 min. A decrease in plasma values of GH, prolactin, TSH, insulin and glucagon and in blood glucose was observed during somatostatin infusion, while FFA levels increased progressively. Plasma IRI and blood glucose increased rapidly when the somatostatin infusion was stopped, while FFA decreased progressively; GH, prolactin, TSH and glucagon remained low as compared to basal levels for one hour after the end of the infusion, i.e. until the end of the experiment. A slight but significant increase of LH and ACTH was observed after the end of the infusion.
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PMID:Pituitary and extrapituitary effects of somatostatin in normal man. 18 9

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 recent discovery of somatostatin-containing cells within the thyroid gland infers that somatostatin may influence thyroid activity. This possibility was investigated by measurements of radio-iodine release in mice pre-treated with 125I and T4. The animals were treated with TSH, isoprenaline or dibutyryl-cyclic AMP with and without concomitant injection of somatostatin. It was found that somatostatin reduced the blood 125I increase in response to each of the three thyroid-stimulating agents. The elimination rates of 125I-labelled T4 and T3 were unaffected by somatostatin. The observations suggests that somatostatin may participate in the regulation of thyroid hormone secretion, by an inhibitory effect exerted within the thyroid gland.
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PMID:Inhibition by somatostatin of mouse thyroid activity following stimulation by thyrotrophin, isoprenaline and dibutyryl cyclic-AMP. 19 13

The anterior pituitary gland of the human fetus has the ability of synthetizing, storing and secreting hormones early during gestation. The patterns of plasma concentrations of hGH, ACTH, LH and FSH during gestation indicate a maximum of secretion at mid-gestation followed by a progressive decrease of these concentrations until term. In contrast, the secretions of PRL and TSH are moderate at mid-gestation and only increase in the last trimester of gestation. Effective control by the central nervous system (CNS) of the pituitary secretions is still immature at mid-gestation. The presence of releasing factors in the fetal hypothalamus has been established (TRF, LRF, somatostatine) and it was postulated that early in life, relatively autonomous and unrestrained secretion of hypothalamic hypophysiotropic releasing factors occurs and, later in development, there was a maturation of inhibitory or restraining influences mediated via the CNS that modulate the secretion of the fetal adenohypophyseal hormones. Observations made with anencephalic newborns confirm that a functional hypothalamus is necessary for the secretions of each of the hormones of the anterior pituitary gland with the exceptiion of PRL, the secretion of which is normal in anencephaly. Although somatostatin probably participates in the regulation of hGH during fetal life, it appears evident that this regulation can only be fully understood with the existence of a GRF (Growth Hormone Releasing Factor).
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PMID:[Hypothalamic factors in the human fetal brain: their role in the ontogeny of fetal hypophyseal functions]. 20 94

In a patient with hypogonadotropic hypogonadism treated with luteinizing hormone releasing hormone (LHRH), secondary failure of both subjective and hormone responses occurred at the time of appearance of binding of 125I-LHRH by the patient's serum. On electrophoresis of the patient's serum with 125I-LHRH, label was found only in the gamma globulin region. 125I-LHRH added to the patient's serum was precipitated by sheep anti-human immunoglobulin G (anti-IgG) but not by sheep anti-human immunoglobulin M (anti-IgM). Competitive displacement of 125I-LHRH by unlabeled LHRH was demonstrated while TSH releasing hormone (TRH), somatostatin and rat pituitary hormones showed no displacement when tested at concentrations 5 X 10(6) greater than that of LHRH. Studies using 14 different analogs of LHRH revealed that those with changes at the carboxy terminus showed binding similar to LHRH. It is concluded that IgG antibody to LHRH was produced in this patient by repeated administration of synthetic LHRH. It is further concluded that antibody specificity is directed toward the N terminus region.
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PMID:Characteristics of antibody produced during chronic treatment with LHRH. 32 67


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