Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immunohistochemical staining for methionine-enkephalin and leucine-enkephalin were used to reveal an enkephalins-like substance in the median eminence and adenohypophysis of guinea pig and rat. Nerve endings were stained for enkephalins in the external layer of the median eminence. By successive staining of two different antigens, somatostatin fibers in the guinea pig were also shown to be enkephalin-immunoreactive. Staining of the adenohypophysis varied with the species and the antisera used. Intermediate lobe and corticomelanotrophs were stained moderately. In both species, and with all the antisera, thyrotrophs were shown to contain an immunoreactive substance. In the guinea pig, gonadotrophs were stained particularly by the anti-leucine-enkephalin antiserum used. The locus of enkephalin action on pituitary functions can be discussed: enkephalins possibly have an inhibiting action on somatostatin fibers, which agrees with the stimulating action of enkephalins on GH already known. Furthermore, enkephalins could have a direct action on pituitary glycoprotein proceducing cells, which would explain their inhibiting action demonstrated previously on LH, FSH and TSH.
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PMID:Immunohistochemical localization of enkephalins in median eminence and adenohypophysis. 37 61

In order to investigate whether somatostatin plays a role in the regulation of thyroid hormone secretion we have compared the effects of a prolonged somatostatin infusion on insulin and glucagon levels, on the one hand, with its effect on T4, T3, rT3 and TSH, on the other. Furthermore, the serum levels of somatomedin A were determined. Saline was infused in control experiments. Cyclic somatostatin was given as an i.v. bolus of 200 micrograms followed by a constant rate infusion of 50 micrograms/h during 24 hours. Somatostatin suppressed basal insulin and glucagon levels as well as insulin responses to meals but did not influence somatomedin A levels. T4 and T3 decreased during the first hour, whether somatostatin was given or not. Thereafter, T4 and T3 remained stable in the control experiments, while they continued to decrease slowly when somatostatin was added. The suppressive effect of somatostatin was significant 11 hours (p less than 0.05) and 24 hours (p less than 0.005) after the onset of the infusion. In contrast, rT3 and TSH were not suppressed by somatostatin. The fact that basal TSH did not decrease, favors the idea that the suppression of T4 and T3 was mainly due to a direct inhibitory effect of somatostatin on the thyroid gland. Our observation that a low dose of somatostatin decreases peripheral T4 and T3 levels supports the idea that somatostatin plays a role in the regulation of thyroid hormone secretion.
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PMID:Effect of 24-hour somatostatin infusion on glucose homeostasis and on the levels of somatomedin A and pancreatic and thyroid hormones in man. 39 78

Hormone responses to a bolus injection of thyrotropin releasing hormone (TRH) were studied in 8 newborn lambs between 6 and 19 hours of age. The effect of a bolus injection and 45 min infusion of somatostatin (SRIF) on these responses was studied in 2 other animals. Serial measurements of serum TSH, prolactin, triiodothyronine (T3) and thyroxine (T4) were conducted for 2 to 6 h in all animals. Mean baseline T4 and T3 concentrations were 12.6 microng/dl and 221 ng/dl, respectively, both significantly higher than values in fetal or adult animals. These high values were due to the events of parturition. In spite of the high baseline T4 and T3 levels, there were rapid and significant increases in both TSH and prolactin concentrations in response to TRH alone. The TSH response evoked further increments in serum T3 and T4 concentrations observed at 30 min and 60 min, respectively, both subsequently increasing progressively through 6 h. During the 45 min period of SRIF infusion, the TSH T4 and T3 responses to the zero time TRH injection were minimal. However, after discontinuing SRIF, late increases in TSH, T4 and T3 were observed. The results indicate that the hyperiodothyroninemia characteristic of the newborn period does not block the response to exogenous TRH, whereas the inhibitory effect of exogenous SRIF is observed in the newborn as in the adult. The increased endogenous TRH secretion presumably responsible for the neonatal TSH surge may be overriding the negative feedback effect of thyroid hormones.
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PMID:The response of newborn sheep to TRH with and without somatostatin. 40 29

Somatostatin levels have been determined by RIA in hypophysial portal blood of pentobarbital-anesthetized male rats. In most animals, immunoreactive somatostatin (SRIF) levels were higher in hypophysial portal blood than in systemic blood. In euthyroid rats, the mean level was 158 +/- 27 pg/ml (n = 8); SRIF was undetectable (less than 30 pg/ml) in systemic blood of these rats. It is suggested that endogenous SRIF was not degraded during the collection of stalk blood, since synthetic SRIF is stable when incubated in rat serum during 4 min at 37 c and 2 h at 0 C, i.e. under the conditions the blood was kept during the collection. SRIF in hypophysial portal plasma had the same immunoreactivity with a specific antiserum against SRIF as did synthetic SRIF. Gel filtration of hypophysial portal plasma revealed two immunoreactive peaks, the major one corresponding to synthetic SRIF, the smaller one representing a larger molecular form. Thyroidectomy and excess of T4 did not modify the levels of SRIF in hypophysial portal blood, suggestinc SRIF is stable when incubated in rat serum during 4 min at 37 C and 2 h at 0 C, i.e. under the conditions the blood was kept during the collection. SRIF in hypophysial portal plasma had the same immunoreactivity with a specific antiserum against SRIF as did synthetic SRIF. Gel filtration of hypophysial portal plasma revealed two immunoreactive peaks, the major one corresponding to synthetic SRIF, the smaller one representing a large molecular form. Thyroidectomy and excess of T4 did not modify the levels of SRIF in hypophysial portal blood, suggesting that the feedback of thyroid hormones on TSH secretion does not involve changes in the secretion of SRIF by the hypothalamus.
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PMID:Immunoreactive somatostatin in rat hypophysial portal blood. 43 85

Intravenous injection of synthetic thyrotropin-releasing hormone (TRH) resulted in a significant and dose-related increase in plasma growth hormone (GH) in the urethane anesthetized rat. The minimum effective does of TRH was 40 ng per 100 g body wt when administered intravenously. The maximum responses of plasma GH to TRH were observed at 5 min following TRH, whereas those of plasma TSH were obtained at 10 min. Pretreatment with either T3 (50 mug/100 g body wt ip) significantly suppressed both plasma GH and TSH responses to TRH. The GH release induced by TRH was significantly inhibited by somatostatin (5 mug/100 g body wt iv) which was injected 5 min and immediately before the injection of TRH.
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PMID:Pasma growth hormone responses to thyrotropin-releasing hormone in the urethane-anesthetized rat. 80 99

Morphine sulfate (MS) and pentobarbital (PB) stimulate growth hormone (GH) release in the rat in vivo, but not from enzymatically dissociated anterior pituitary cells in vitro. Somatostatin and thyrotropin-releasing factor (TRF) inhibit the in vivo release of GH induced by MS, with 50% inhibition at ca. 2.3 and 4.6 mug/100 g BW, respectively. Somatostatin and TRF similarly inhibit PB-induced GH release. Prostaglandin E2 stimulates GH release both in vivo and in vitro. Both of these responses are inhibited by somatostatin (50% inhibition at ca. 10 mug/100g BW), but neither is altered by TRF (100 mug/100g BW). Both normal and hypophysectomized rats receiving MS exhibited a rapid vibration of the tail immediately after administration of TRF (30 mug/100g BW). Structural analogs of TRF with low TSH-releasing activity did not inhibit GH release nor induced tail vibration in MS-treated rats. Pyroglutamyl-3-methyl-histidyl-prolinamide, with 8 times the hypophysiotropic potency of TRF, is similarly more potent than TRF in inhibiting GH release and inducing tail vibration in MS-treated rats. These results suggest the following: 1) MS and PB act at a central nervous system (CNS) site to release GH; 2) TRF may act at a CNS site to inhibit MS- and PB-induced GH release; 3) somatostatin has direct pituitary effects on inhibition of GH, but a CNS site of action cannot be excluded; and 4) TRF stimulates tail motor activity in MS-treated rats.
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PMID:Growth hormone release in the rat: effects of somatostatin and thyrotropin-releasing factor. 81 Mar 43

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

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 prolactin (PRL)-releasing activity of porcine stalk median eminence (pSME) was characterized by an in vivo bioassay and concomitant radioi-munoassay of plasma PRL and thyrotropin (TSH) levels. Methanol extracts of pSME stimulated PRL release in 3-day estrogen-primed rats when administered by the intracarotid route in doses ranging from 0.1 to 2.0 pSME equivalents. Synthetic thyrotropin-releasing hormone (TRH) stimulated the release of PRL and TSH in the dose range of 10 to 300 ng. PRL release was greater in response to a maximally effective dose of pSME than the release elicited by a maximal dose of TRH, and pSME administered together with a greater than mazimally effective dose of TRH caused additional PRL but not TSH secretion. Lysine vasopressin and prostaglandin E1 and E2 stimulated PRL release only at doses several orders of magnitude greater than the dose present in pSME. Somatostatin inhibited the release of TSH but not that of PRL whether the stimulus employed was pSME or TRH. The effective inhibitory dose of somatostatin was also significantly greater than the reported hypothalamic content. When pSME was subjected to incubation with plasma, a treatment reported to inactivate TRH, TSH-releasing activity was destroyed to a greater extent than was PRL-releasing activity. When pSME was adsorbed onto charcoal, the supernatant solution was devoid of TRH, as determined by complete removal of a [3H]TRH marker, yet substantial PRL-releasing activity was retained. TSH-releasing activity eluted from the charcoal with methanol was considerably greater than that expected on the basis of the recovery of [3H]TRH, suggesting the presence in the crude extract of a TSH-release inhibitor or of a TSH-releasing factor other than TRH. Based on the above evidence, we conclude that crude pSME contains PRL-releasing substance(s) distinct from the tripeptide TRH.
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PMID:Dissociation of prolactin-releasing activity from thyrotropin-releasing hormone in porcine stalk median eminence. 81 52


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