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)

TRH and a new TRH analog (all L-pyro-2-aminoadipyl-histidyl-thiazolidine-4-carboxamide, MK-771) have been compared with several other peptides for their "analeptic" activity and their ability to enhance the excitatory actions of microiontophoretically applied acetylcholine (ACh) on cerebral cortical neurons of rats. TRH and MK-771 offset the narcosis induced by pentobarbital in mice, whereas the C-terminal free acid derived from TRH, melanostatin, somatostatin and pyroglutamyl-histidineamide have been found inactive. Similarly, of these peptides only TRH and MK-771 induced a tremor of the forepaws in pentobarbital-anesthetized mice. Employing comparable ejection currents and durations, only TRH and MK-771, applied by microiontophoresis, enhanced the excitatory actions of ACh on spontaneously active cortical neurons in anesthetized rats. Based on these findings and other recent data, it is suggested that the interactions of TRH and MK-771 with cholinergic mechanisms may underlie some of the actions, including their anti-anesthetic effects, of these peptides.
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PMID:Studies on the neuropharmacology of thyrotropin releasing hormone (TRH) and a new TRH analog. 41 61

Somatostatin, at concentrations up to 10(-7) M, does not inhibit the basal release of TSH from primary cultures of rat anterior pituitary cells. The TRH-induced TSH release is however 65% reduced by somatostatin, half-maximal inhibition being measured at 2.5 x 10(-10) M somatostatin. The concentration of TRH giving half-maximal stimulation (ED50) of TSH release is only slightly increased from 1 to 3 x 10(-9) M in the presence of 10(-8) M somatostatin. Somatostatin inhibits by 45-65% both the basal and TRH-induced PRL release of pituitary cells prepared from adult female rats, with half-maximal inhibition at approximately 5 x 10(-10) M somatostatin. The TRH ED50 for PRL release was not significantly affected by somatostatin. Somatostatin (200 mug) has no effect on the basal plasma levels of TSH or PRL in anesthetized male rats treated with estradiol benzoate (EB), hypothyroid rats, or hypothyroid animals treated with EB. The plasma TSH response to TRH is, however, reduced by approximately 75% by somatostatin while the plasma PRL response is not affected by injection of the peptide. The interaction between TRH and somatostatin for both TSH and PRL release is non-competitive and is thus likely to occur at a step subsequent to the binding of the peptides to their specific receptors in both thyrotrophs and mammotrophs.
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PMID:Characteristics of the interaction between thyrotropin-releasing hormone and somatostatin for thyrotropin and prolactin release. 81 94

The reaction products of plasma enzyme degradation of TRH were identified by thin layer chromatography. The enzyme in normal rat plasma yields proline and pGlu-His as major reaction products. High concentrations of proline decrease peptide cleavage, resulting in greater amounts of acid TRH. The apparent Km of the enzyme is 4.1 X 10(-6) M. LHRH and neurotensin are competitive inhibitors with Ki of 5 X 10(-6) M and 1.5 X 10(-5) M, respectively. Somatostatin, MIF, oxytocin, arg-vasopressin, arg-vasotocin, neurophysin II and glucagon do not compete; and pGlu-His-Pro-OH, Glu-His-Pro-OH, pGlu-His, His-Pro-NH2, and Pro-NH2 do not affect enzyme activity. These data suggest that the substrated requires pGlu and a terminal or internal amide to complex with the enzyme. The enzyme is markedly inhibited by Cu++, Bal, benzamadine, p-(chloromercuri)-benzoic acid, moderately affected by EDTA and puromycin, and unaffected by mercaptoethanol. TSH does not affect enzyme activity while LH inhibits it moderately at high concentrations (300-600 pg/ml).
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PMID:Characteristics of the plasma TRH-degrading enzyme. 81 19

Specificity of the effect of prostaglandins (PGs) on hormone release by the anterior pituitary gland was studied using cells in primary culture. Growth hormone (GH) release is stimulated by all eight PGs studied, PGE1 and E2 being 1000-fold more potent than the corresponding PGFs. The release of luteinizing hormone (LH), follicle-stimulating hormone (FSH), and prolactin (PRL) remains unchanged upon addition of PGEs. While the basal release of thyrotropin (TSH) is only slightly stimulated by concentrations of PGEs above 10(-6)M, an important potentiation of the stimulatory effect of thyrotropin-releasing hormone on TSH release is observed. The release of GH, TSH and LH is stimulated equally well by PGAs and PGBs at concentrations higher than 10(-6)M, 3 X 10(-6)M, and 10(-5)M, respectively. PGFs do not affect the release of any of the measured pituitary hormones at concentrations below 10(-4)M. The stimulation of GH release by PGE2 can be inhibited by the PG antagonist 7-oxa-13-prostynoic acid, a half-maximal inhibition being found at a concentration of 4 X 10(-5)M of the antagonist in the presence of 10(-6)M PGE2. In the presence of somatostatin 10(-8)M, the inhibition of GH release cannot be reversed by PGE2 at concentrations up to 10(-4)M. 8-bromo-cyclic AMP-induced GH release is additive with that produced by PGE2. The present data show that 1) of the five pituitary hormones measured, only GH release is stimulated by prostaglandins at relatively low concentrations, 2) the PGE-induced GH release can be competitively inhibited by 7-oxa-13-prostynoic acid, 3) the inhibition of GH release by somatostatin cannot be reversed by PGE2 and 4) the PGEs increase the responsiveness of the thyrotrophs to TRH.
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PMID:Specificity of the stimulatory effect of prostaglandins on hormone release in rat anterior pituitary cells in culture. 81 70

Passive immunization of rats with an antiserum to synthetic somatostatin caused a 250% elevation of basal serum TSH levels and a nearly 200% increase in TSH-response to TRH. These findings strongly support the concept that pituitary thyrotrophs are regulated by endogenous somatostatin as well as by TRH and thyroid hormones. Serum GH levels in the antiserum-treated rats were considerably higher than those in rats which received normal serum. No clearcut influence on prolactin secretion was observed.
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PMID:Increase in basal and thyrotropin-releasing hormone (TRH)-stimulated secretion of thyrotropin (TSH) by passive immunization with antiserum to somatostatin in rats. 81 48

The infusion of linear somatostatin did not block prolactin release induced by either perphenazine, TRH or serotonin. Somatostatin infusion, however, potentiated prolactin release induced by perphenazine and TRH but not that induced by serotonin.
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PMID:The influence of somatostatin on drug-induced prolactin release in the monkey. 82 78

Thirteen patients with acromegaly were subjected to the examination of autonomity in growth hormone (GH) secretion. TRH (500 mug iv), arginine (0.5 g/kg of body weight iv infusion), LH-RH (100 mug iv) and L-dopa (500 mg orally) were administered, and plasma GH was measured. Among them, 11 patients showed some response in plasma GH to at least one agent, but the other 2 cases showed no response to any of the above 4 agents. In the former 11 cases, the patients were regarded as belonging to the less autonomous type and in the latter 2, to the more autonomous type in GH secretion. Six cases (4 cases of the less autonomous and 2 cases of the more autonomous type) received an administration of 500 mug of synthetic somatostatin parenterally. Following administration of somatostatin, the patients of both types showed significant GH decrease, although GH decrease in the more autonomous type was smaller than that of the less autonomous type. These results would suggest that there might be no acromegalics secreting GH FROM THE PITUITARY WITH COMPLETE AUTONOMITY, AND THE DIFFERENCE OF AUTONOMITY IN ACROMEGALIC PATIENTS MIGHT DEPEND EITHER ON THE DIFFERENCE IN SENSITIVITY AND/OR THE NUMBER OF RECEPTORS IN THE PITUITARY RATHER THAN THOSE IN HYPOTHALAMUS TO EXOGENOUS STIMULI.
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PMID:Differences in autonomity of growth hormone secretion in patients with acromegaly. 82 58

The studies described were performed to develop a technically simple, yet sensitive in vivo model for growth hormone (GH) releasing activity in porcine stalk median eminence (pSME) extracts, to compare the GH releasing effects of pSME with those of prostaglandin E2 (PGE2), and to study the effect of somatostatin (SRIF) on the above stimuli. The use of the one day estrogen-primed male rat in conjunction with intracarotid injection of test materials provided a model sensitive to the injection of one pSME. Neither increasing the duration of estrogen pre-treatment nor reserpine resulted in a greater response. The GH releasing effects of pSME were directly related to the preinjection GH level. Two successive injections of pSME at 30 minute intervals evoked similar responses. In contrast, PGE2 effects were not potentiated by estrogen pre-treatment and were independent of the preinjection GH level. The GH releasing effect of pSME was not related to its content of TRH or K+. Extracts of porcine cerebral cortex also contained GH releasing activity, although at a lower concentration than in pSME. Somatostatin inhibited the GH releasing effects of pSME, PGE2, and cerebral cortex extract. These results provide evidence for the direct inhibitory effect of SRIF on GH secretion in vivo and suggest that SRIF is capable of blocking a variety of different stimuli to GH release.
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PMID:Effects of porcine stalk median eminence and prostaglandin E2 on rat growth hormone secretion in vivo and their inhibition by somatostatin. 109 73

Two studies were performed to determine the importance of endogenous somatostatin (SS) in regulating human TSH secretion. In the first, healthy adult males were studied in random order on two occasions a week apart. They were infused with either saline to maintain euglycaemia, or 10% dextrose to raise blood glucose concentration by at least 3 mmol/L within 10 minutes, and cause hypothalamic SS release. Fifteen minutes after the infusions were commenced, 200 micrograms of TRH was injected intravenously and TSH release was followed for the next 75 minutes. In the second study, persons with elevations of TSH to between 3 and 12 mU/L were also infused with either saline or 10% dextrose. Infusions were continued for 1 hour and the TSH secreted was measured over this time period. There was no significant difference between the euglycaemic or hyperglycaemic studies in TRH-induced TSH secretion, either as areas under the curve, or as mean values at individual times. Mean TSH peaks were seen in both groups at 25 minutes post-TRH. Mean peak values were 8.11 +/- 0.97 mU/L (mean +/- SEM) in the euglycaemic group, and 7.94 +/- 1.18 mU/L in the hyperglycaemic group. Mean area under the curve was 396.3 +/- 53.2 mU/L/75 mins (SEM) for the euglycaemic study and 385.1 +/- 59.5 mU/L/75 mins (SEM) for the hyperglycaemic group. In the infusion study in the persons with mild hypothyroidism, there was no difference in TSH concentration between the two infusion regimes. These results show that in acute studies, hyperglycaemia does not inhibit human TSH release, despite the likelihood of hypothalamic-pituitary SS concentration being increased.
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PMID:The effect of endogenous somatostatin upon human thyrotrophin (TSH) secretion. 134 94

Somatostatin (SS) inhibits GH and TSH secretion, but its role in modulating their pulsatility is unclear. We studied GH and TSH responses to GH-releasing hormone (GHRH) and TRH stimulation upon a variable background infusion of saline, SS-(1-14) at 20 and 100 micrograms/m2.h, and oral pyridostigmine (30 and 60 mg) in six adult males. Basal GH levels were unaffected by SS-(1-14). Deconvolution analysis of serum GH values demonstrated that the pituitary responded to two GHRH stimuli 90 min apart without attenuation of the second response. The higher dose of SS-(1-14) significantly blunted the first GH response; second GH responses were further attenuated by both SS-(1-14) doses. Maximum GH release and "switch-off" rates for both stimuli were reduced without changes in the 50% secretion time. Pyridostigmine enhanced the first GH response to GHRH with an increase in the GH release rate; second GH responses were not augmented. GH secretion was prolonged by pyridostigmine, although the 50% secretion time remained unchanged. Peak stimulated serum TSH was attenuated by both SS-(1-14) doses, but pyridostigmine had no effect. All other TSH parameters examined were unaffected. We conclude that the GH response to GHRH is dependent on SS tone, but that the thyrotroph is not tonically inhibited by SS. SS attenuates the rate of GH release without changing the duration of secretion and appears important in terminating GH secretion.
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PMID:The effect of changing somatostatin tone on the pituitary growth hormone and thyroid-stimulating hormone responses to their respective releasing factor stimuli. 135 4


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