Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Physiological and pharmacological evidence has suggested that both endogenous opiates and gonadotropin-releasing hormone (GnRH) itself can act centrally to exert a tonic inhibition on gonadotropin secretion via an inhibition of the neurosecretion of GnRH. To determine if the effects of these two peptides might be mediated via a direct synaptic input to the GnRH neuron, we undertook a double label ultrastructural study. We were able to localize in the same tissue section beta-endorphin and GnRH. Analysis of serial sections through GnRH perikarya and dendrites in the male rat diagonal band/preoptic area revealed that almost 10% of the synapses impinging on the GnRH neuron contained beta-endorphin; an additional 10% of the terminals contained GnRH. These data provide anatomical evidence in support of both a direct modulation of GnRH release by opiates and of the presence of an ultrashort feedback loop.
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PMID:beta-Endorphin and gonadotropin-releasing hormone synaptic input to gonadotropin-releasing hormone neurosecretory cells in the male rat. 267 Oct 62

Recombinant human interleukin-1 beta (IL-1 beta) significantly increased prostaglandin E2 (PGE2) in a dose-dependent manner in rat astrocyte culture. The minimum effective dose of IL-1 beta was 10(-10)M. IL-1 alpha also increased PGE2, but at a higher concentration. The minimum effective dose of IL-1 alpha was 10(-8)M, indicating it to be 100-fold less effective than IL-1 beta. On the other hand neither IL-1 beta nor IL-1 alpha increased PGE2 production by neuron cultures at any concentration tested. PGE2 response to IL-1 beta was suppressed by simultaneous addition of CRH, somatostatin-14 and LHRH, while these neuropeptides alone did not alter the basal PGE2 levels. Substance P, vasoactive intestinal polypeptide and alpha-MSH altered neither basal nor IL-1 beta-induced increase in PGE2 levels. Angiotensin II (AII) alone also increased PGE2 in cultured astrocytes. Combined addition of AII and IL-1 beta induced a synergistic effect in increasing PGE2 levels. The direct action of IL-1 beta on astrocyte culture suggests that astrocytes may be the target cells for IL-1 beta in the central nervous system. In view of the essential role of central PGE2 in IL-1 beta-induced CRH/ACTH release, these findings suggest the presence of a sophisticated regulatory network in the immune-neuroendocrine interaction.
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PMID:Interleukin-1 beta increases prostaglandin E2 in rat astrocyte cultures: modulatory effect of neuropeptides. 278 13

The paper is concerned with the results of a study of the level of plasma ACTH, cortisol and prolactin before and after i. v. injection of LHRH to 20 patients with Itsenko-Cushing disease and to 5 healthy persons. In healthy persons LHRH injection caused no significant changes in the level of plasma ACTH, cortisol and prolactin. Patients with Itsenko-Cushing disease who had a high basal level of corticotropin on the 30th min after i.v. LHRH injection demonstrated a significant increase in the hormone level. A response to LHRH injection was absent in patients with a normal basal level of corticotropin and in healthy persons. A statistically significant increase in cortisol concentration was noted on the 60th min after LHRH injection in some of the patients responding to LHRH by a high ACTH level. LHRH injection was not accompanied by significant changes in the level of plasma prolactin in either of the subgroups.
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PMID:[Dynamics of the corticotropin, cortisol and prolactin content of the blood plasma of women with Itsenko-Cushing disease administered luliberin]. 282 33

Six normal and 8 neoplastic adrenal medullae were assayed for several immunoreactive (IR) proopiomelanocortin (POMC) and hypothalamic peptides. IR-POMC peptides were found in normal and tumor tissue in concentrations ranging from 0.0003 to 0.1% of those in pituitary. Their molecular sizes resembled those of pituitary intermediate lobe POMC peptides. No intact POMC was found. One pheochromocytoma contained fully bioactive IR-adrenocorticotropic hormone (IR-ACTH; Mr approximately 4,500) and an intermediate-sized (Mr approximately 10,000) IR-ACTH with approximately 69% bioactivity. Normal and tumorous medullae contained IR-corticotropin-releasing hormone (CRH) in concentrations ranging from 0.6 to 4% of those in hypothalamus except for one pheochromocytoma that contained 40 times that amount of IR-CRH, which was chromatographically indistinguishable from hypothalamic CRH and fully bioactive. IR-somatostatin and IR-growth hormone-releasing hormone were found in both tissue types, but IR-gonadotropin-releasing hormone and IR-thyrotropin-releasing hormone (TRH) were not, although IR-histidyl-proline diketopiperazine, a putative TRH metabolite, was found. IR-arginine vasopressin was found in two normal medullae, but not in pheochromocytomas.
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PMID:Pituitary and hypothalamic hormones in normal and neoplastic adrenal medullae: biologically active corticotropin-releasing hormone and corticotropin. 282 21

The effect of cortisol or adrenocorticotropic hormone (ACTH) on basal and gonadotropin-releasing hormone (GnRH)-induced secretion of luteinizing hormone (LH) was studied in vitro using dispersed pig pituitary cells. Pig pituitary cells were dispersed with collagenase and DNAase and then grown in McCoy's 5a medium containing 10% dextran charcoal-pretreated horse serum and 2.5% fetal calf serum for 3 days. Cells were preincubated with cortisol or ACTH before GnRH was added. When pituitary cells were incubated with 400 micrograms cortisol/ml medium for 6 h or longer, increase basal secretion of LH was observed. However, GnRH-induced LH release was reduced by cortisol. The degree of this reduction was dependent on cortisol, and a concentration of cortisol higher than 100 micrograms/ml was needed. Cortisol also inhibited the 17 beta-estradiol-induced increase in GnRH response. ACTH-(1-24), ACTH-(1-39), or porcine ACTH had no influence on GnRH-induced LH secretion. Our results show that cortisol can act directly on pig pituitary to inhibit both normal and estradiol-sensitized LH responsiveness to GnRH.
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PMID:Effect of cortisol or adrenocorticotropic hormone on luteinizing hormone secretion by pig pituitary cells in vitro. 282 56

In vitro and in vivo perfusion techniques were used to examine the changes in the release of beta-endorphin, methionine-enkephalin (met-enkephalin), dynorphin and luteinizing hormone releasing hormone (LHRH) in response to the corticotropin releasing factor (CRF) receptor antagonist, alpha-helical CRF9-41. All four peptides were measured in the same sample collected at each time interval by specific radioimmunoassay methods. In vitro release experiments were conducted using slices of hypothalami obtained from male rats whereas the in vivo release of these peptides was assessed in push-pull perfusates of the arcuate-median eminence (ARC-ME) region of the medial basal hypothalamus of chloral hydrate-anaesthetized male rats. Treatment of rat hypothalamic slices in vitro with alpha-helical CRF9-41 (10(-6) M) resulted in a significant suppression of the release of beta-endorphin and met-enkephalin within 10 min of application of the antagonist and a coincident significant increase in the release of LHRH. The levels of dynorphin were reduced but these changes were not significant. Within 10 min of withdrawal of the receptor antagonist and perfusion with normal (antagonist-free) medium the levels of these peptides returned to pretreatment values, i.e. the levels of beta-endorphin, met-enkephalin and dynorphin rose while those of LHRH fell. Comparable results were obtained in vivo during push-pull perfusion of the ARC-ME region with alpha-helical CRF9-41.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Concomitant changes in the in vitro and in vivo release of opioid peptides and luteinizing hormone-releasing hormone from the hypothalamus following blockade of receptors for corticotropin-releasing factor. 284 Jun

The effects of several hypothalamic peptides on hormone secretion by pituitaries of three species of anuran amphibians were investigated using in vitro techniques. Secretion of thyrotropic bioactivity (designated thyrotropin or TSH) was quantified by bioassay of the pituitary incubation medium using thyroxine (T4) production by paired thyroids from the same animals. Pituitaries from adult male Rana pipiens were cultured in medium alone, 10 or 100 ng/ml thyrotropin-releasing hormone (TRH), 1000 ng/ml ovine corticotropin-releasing hormone (oCRH), or 300 ng/ml synthetic mammalian gonadotropin-releasing hormone (mGnRH) (these represent approximately equimolar doses) for two 2-hr incubation periods. TSH secretion by control glands was nondetectable, but glands exposed to TRH increased their secretion of TSH in a dose-dependent manner. Both oCRH and mGnRH also stimulated significant increases in TSH. oCRH produced greater output of TSH than did the other two peptides and mGnRH was less active than TRH. Secretion of immunoreactive gonadotropin (GtH) was increased by mGnRH, but not by the other two peptides. Pituitaries from two other anuran species, Hyla regilla and Xenopus laevis, also responded to 100 ng/ml TRH by releasing TSH. These results provide the first unequivocal evidence that TRH can act directly on the anuran amphibian pituitary to stimulate the secretion of TSH, and suggest that the presence of functional TRH receptors on pituitary thyrotropes may be of greater phylogenetic antiquity than has been assumed previously. Furthermore, these data suggest the potential for multihormonal control of TSH secretion in frogs.
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PMID:Several hypothalamic peptides stimulate in vitro thyrotropin secretion by pituitaries of anuran amphibians. 285 81

[125I-Tyr]Somatostatin [( 125I-Tyr]SRIH) binding was found in 11 GH-secreting pituitary adenomas [Kd = 0.46 +/- 0.15 (+/- SE) nM; maximum binding, 165 +/- 35 fmol/mg protein). This binding was specific, since it was displaced by somatostatin-14 (SRIH-14), N-Tyr-SRIH-14, and SRIH-28. In contrast, a number of peptides and drugs not structurally related to SRIH, such as bombesin, dopamine, LHRH, met-enkephalin, naloxone, neurotensin, secretin, substance P, TRH, or vasoactive intestinal peptide, did not affect [125I-Tyr]SRIH binding. [125I-Tyr]SRIH specific binding also was found in PRL-secreting pituitary adenomas. The kinetic characteristics of the specific binding were similar to those of GH-secreting adenomas. However, maximal binding was one quarter that of GH-secreting adenomas (37 +/- 9 fmol/mg protein). In contrast, nonsecreting (chromophobe) tumors were devoid of any specific binding. Finally, in acromegaly, the density of [125I-Tyr]SRIH-binding sites in the adenomas was negatively correlated with plasma GH levels before surgery (r = -0.80). This suggests that somatostatinergic control is involved in GH secretion in acromegalic patients.
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PMID:Somatostatin receptors in human growth hormone and prolactin-secreting pituitary adenomas. 286 Jan 20

A possible functional relationship between corticotropin-releasing factor (CRF) and opiate peptide neuronal systems (beta-endorphin, dynorphin1-17 and Met-enkephalin) and their interactions with gonadotropin releasing hormone (GnRH) in the mesencephalic central gray (MCG) for the regulation of lordosis behaviour was assessed in ovariectomized, oestrogen-treated and oestrogen-progesterone-treated female rats. Lordosis behaviour triggered by male mounting was inhibited in a dose-dependent fashion by CRF microinfused into the MCG in both oestrogen-treated and oestrogen-progesterone-treated female rats. This CRF-induced inhibition of lordosis could be overcome by a pre-infusion of naloxone or anti-beta-endorphin-globulin (anti-beta-end-G) directly into the MCG but not by anti-Met-enkephalin globulin (anti-enk-G) or anti-dynorphin1-17 globulin (anti-dynor-G). Supporting data indicate that the facilitation of lordosis behaviour induced by treatment with naloxone or anti-beta-end-G alone but not with anti-enk-G or anti-dynor-G may be due to enhanced GnRH release. This results from the action of these substances in overcoming the inhibition of GnRH secretion mediated specifically by beta-endorphin but not by Met-enkephalin or dynorphin1-17 in the MCG. These studies together with previous data showing that GnRH can overcome the abolition of lordosis by beta-endorphin in the MCG, indicate a close relationship between beta-endorphin (but not Met-enkephalin or dynorphin) and GnRH systems in the MCG in the control of lordosis behaviour. Thus, the inhibition of lordosis by CRF and the complete reversal of this blockade by naloxone or anti-beta-end-G may suggest that CRF could enhance the release of beta-endorphin from fibres in the MCG; beta-endorphin then inhibits lordosis by inhibiting the release of GnRH. However, a direct inhibitory effect of CRF on GnRH release is also likely since anti-CRF-gamma-globulin (anti-CRF-G) infused into the MCG produced a long-lasting facilitation of lordosis which can be blocked by an antagonist analogue of GnRH; in addition, previous studies have shown that GnRH infused into the MCG completely overcame the CRF-induced abolition of lordosis and potentiated lordosis to high levels. These results suggest that there may be functional neuroanatomical relationships between CRF, beta-endorphin and GnRH neuronal systems in the MCG in the control of female sexual behaviour. Neither Met-enkephalin nor dynorphin1-17 appear to participate in such mechanisms.
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PMID:Modulation of lordosis behaviour in the female rat by corticotropin releasing factor, beta-endorphin and gonadotropin releasing hormone in the mesencephalic central gray. 286 Sep 50

Rat anterior pituitary quarters or acutely dispersed rat anterior pituitary cells were incubated in vitro, and the release of dynorphin A1-13-like immunoreactivity (Dyn A1-13-IR) into the incubation medium was studied. Addition of LHRH led to a concentration-dependent enhancement of the release of Dyn A1-13-IR with a maximum secretory rate which was about 4-fold higher than basal secretion. Dyn A1-13-IR was released by LHRH concomitantly with LH and FSH, and the concentration-response relationships as well as the time course were virtually identical. Gel filtration and HPLC revealed a single peak of Dyn A1-13-IR, with an apparent mol wt of about 6000. In addition to Dyn A1-13-IR, alpha-neo-endorphin-like immunoreactivity was released by LHRH. The LHRH-stimulated release of Dyn A1-13-IR was mimicked by the LHRH analog D-Ala6,des-Gly10-LHRH ethylamide and blocked in a competitive manner by the LHRH antagonist D-pGlu1,D-Phe2,D-Trp3,6-LHRH. Addition of TRH (5 microM), rat corticotropin-releasing factor (100 nM), arginine vasopressin (1 microM), or synthetic human pancreatic GH-releasing hormone (10 nM) produced no effect on Dyn A1-13-IR release. An extract of the rat medial basal hypothalamus stimulated the release of Dyn A1-13-IR and beta-endorphin-like immunoreactivity, and the former, but not the latter, effect was blocked by the LHRH antagonist D-pGlu1,D-Phe2,D-Trp3,6-LHRH. These results demonstrate that dynorphin-like material and other proenkephalin B-derived peptides are released concomitantly with LH and FSH from rat adenohypophysis in vitro upon activation of LHRH receptors. This may indicate that proenkephalin B-derived peptides coexist with LH and/or FSH in at least some gonadotrophs of the normal rat anterior pituitary gland.
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PMID:Corelease of dynorphin-like immunoreactivity, luteinizing hormone, and follicle-stimulating hormone from rat adenohypophysis in vitro. 286 8


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