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)

Arachidonic acid metabolites have been shown to modulate the secretion of various hormones, including luteinizing hormone, growth hormone and adrenocorticotropin. In this paper we describe the effect of a series of eicosanoids on hypothalamic secretion of corticotropin-releasing hormone (CRH) in vitro. Explanted rat hypothalami in culture were exposed to prostaglandins (PG) F2 alpha or E2, thromboxane (TX) B2, the TXA2 receptor agonist U-49,619 and leukotrienes (LT) B4, C4 and D4 at concentrations ranging from 10(-15) to 10(-5) M. PGE2, LTD4 and TXB2 did not alter hypothalamic CRH secretion. On the other hand, the remaining eicosanoids tested induced a significant increase of hypothalamic CRH secretion (p less than 0.05). The concentration of 10(-11) M dexamethasone inhibited the effect of stimulatory eicosanoids on CRH secretion. The CRH response to U-49,619 was completely prevented by the TXA2 receptor antagonist SQ-29,548. The latter also inhibited serotonin (5-HT)-, acetylcholine (ACh)- and PGF2 alpha-induced CRH release. Indomethacin was capable of blocking the secretion of CRH induced by 5-HT and ACh. In addition, PGE2 inhibited the increase of CRH secretion induced by PGF2 alpha, 5-HT and ACh. These findings suggest that eicosanoids may be involved in the regulation of hypothalamic CRH secretion, either as autocrine/paracrine or as endocrine factors.
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PMID:Arachidonic acid metabolites modulate rat hypothalamic corticotropin-releasing hormone secretion in vitro. 255 44

The stress-responsive neuropeptide beta-endorphin (beta-END) has been shown to either enhance or suppress interferon-gamma (IFN-gamma) production by mitogen stimulated peripheral blood mononuclear cells (PBMNC) in vitro. In this study, we investigated whether donor selection and the medium used for cell culture influenced the modulatory effect of beta-END on the IFN-gamma production by PBMNC. Considerable variation of the effect of beta-END on IFN-gamma production was observed in individuals who underwent multiple testing. Suppression of IFN-gamma was significantly greater in 16 male donors (29 +/- 6.0%) compared to 8 female donors (1.5 +/- 6.4%) when PBMNC were preincubated for 3 h with beta-END followed by concanavalin A stimulation for 72 h in medium containing 20% fetal bovine serum (FBS). Lowering the concentration of FBS resulted in enhanced production of IFN-gamma by PBMNC exposed to beta-END. Arachidonic acid or beta-END added separately to medium containing 3% autologous serum produced no suppression of IFN-gamma, but when added together resulted in significant suppression. This observation provides support for the hypothesis that beta-END achieves its suppressive effect on IFN-gamma via a mechanism involving arachidonic acid metabolism. We conclude that the modulatory effect of beta-END on IFN-gamma production by PBMNC is both donor and medium dependent.
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PMID:Modulatory effects of beta-endorphin on interferon-gamma production by cultured peripheral blood mononuclear cells: heterogeneity among donors and the influence of culture medium. 297 92

Arachidonic acid is liberated from phospholipids by various hypothalamic releasing hormones and may be involved in stimulus-secretion coupling in rat adenohypophysis. In the present study, the effect of exogenous arachidonic acid on calcium homeostasis in rat anterior pituitary cells was investigated in vitro. Arachidonic acid markedly stimulated the release of various anterior pituitary hormones (beta-endorphin, luteinizing hormone, growth hormone). Arachidonic acid (10 mumol/l) decreased the initial rate of 45Ca2+ uptake. In cells prelabelled with 45Ca2+, arachidonic acid (10 mumol/l) decreased the exchangeable cell calcium content and increased the rate of 45Ca2+ extrusion. Cytosolic free calcium concentration [( Ca2+]i) was measured with the fluorescent indicator fura-2. Arachidonic acid markedly elevated [Ca2+]i. The concentration dependency of this effect (1 mumol/l and above) was similar to that on hormone secretion. Arachidonic acid (6 mumol/l) elevated [Ca2+]i by about 300 nmol/l, and arachidonic acid (10 mumol/l) raised [Ca2+]i into the micromolar range. The effect of arachidonic acid (3 mumol/l) on [Ca2+]i was not influenced by inhibitors of arachidonic acid metabolism (nordihydroguaiaretic acid, BW755C). In Ca2+-free media (Ca2+ omitted, EGTA 2 mmol/l), the effect of arachidonic acid (3 mumol/l) on [Ca2+]i was almost unimpaired, whereas the effect of arachidonic acid (10 mumol/l) was reduced. Thus, the secretagogue arachidonic acid induces calcium mobilization and an increase in cytosolic free calcium concentration. These actions further qualify arachidonic acid as a potential intracellular mediator of stimulus-induced hormone secretion from rat adenohypophysis.
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PMID:Arachidonic acid elevates cytosolic free calcium concentration in rat anterior pituitary cells. 314 79

The melanosome dispersing activity of prostaglandins PGE1, PGE2, PGF1 alpha, PGF2 alpha, PGI2 and 6 beta PGI, was tested on the melanophores of Anolis carolinensis. Only PGE2 and PGE1 were active and while PGE2 was the most potent and acted synergistically with alpha-MSH, PGE1 was additive with alpha-MSH. Arachidonic acid also stimulated melanosome dispersion but its effect was blocked by indomethacin suggesting an action through its conversion to PGE1 or PGE2. The effect of alpha-MSH, on the other hand, was unaltered by indomethacin which suggests that alpha-MSH stimulated melanosome dispersion does not depend upon prostaglandin synthesis. Thus, while some prostaglandins may interact with alpha-MSH to stimulate melanosome dispersion they are unlikely to mediate its action.
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PMID:The stimulatory effects of prostaglandins on the melanophores of the lizard, Anolis carolinensis. 391 35

1. The modulator effects of a series of neurotransmitters and related substances were tested on responses to adenosine 5'-triphosphate (ATP) at a recombinant P2x2 receptor expressed in defolliculated Xenopus oocytes. 2. Nicotine, 5'-hydroxytryptamine (5-HT), noradrenaline, adenosine, bradykinin and histamine (all 100 microM) potentiated the responses to ATP (3 microM). an effect found due to acidification of the bathing solution by these drugs. 3. Arachidonic acid, met-enkephalin, substance P, calcitonin gene-related peptide (CGRP) (all 100 microM) and nerve growth factor (NGF; 50 ng ml-1) potentiated the responses to ATP (3 microM) through a largely or wholly pH-independent effect. 4. Small acidic and alkaline shifts, as little as 0.03 pH-units, enhanced or diminished the responses to ATP, respectively. A linear relationship existed between the degree of potentiation of the ATP-induced responses caused by nicotine, 5-HT, noradrenaline, adenosine, bradykinin and histamine and the potentiation of these responses induced by the addition of acid to the superfusate. 5. Since P2x receptors on sensory neurones include P2x2 subunits, the attendant acidosis and ATP-release associated with tissue injury may play a role in sensitizing sensory nerve fibres.
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PMID:Potentiation of ATP-responses at a recombinant P2x2 receptor by neurotransmitters and related substances. 911 13

The biochemical basis of the short-term inhibitory effects of glucocorticoids on corticotropin release from pituitary corticotrophs is still obscure. A well-characterized effect of glucocorticoids in several cell types is the inhibition of arachidonic acid (AA) generation by phospholipase A2 (PLA2). Arachidonic acid and its metabolites have been implicated in the secretory process from a number of pituitary cells, such as the corticotrophs. We have thus examined the role of AA in the anti-secretagogue effects of glucocorticoids in a corticotropin-secreting clonal corticotroph line (AtT-20 D16/16). Glucocorticoids decreased AA release induced by melittin, a bee venom protein related to extracellular PLA2. When a possible role of AA in corticotropin release was studied, the following results were obtained: (a) all corticotropin secretagogues tested, including corticotropin-releasing factor (CRF), did not alter AA generation; (b) calcium and guanine nucleotides, which stimulate corticotropin release in permeabilized cells, inhibited the release of AA under the same conditions; (c) administration of melittin or of exogenous AA had no effect on basal and CRF-stimulated corticotropin release; (d) administration of large amounts of exogenous AA was unable to restore the ability to secrete corticotropin under suppression by glucocorticoids. Altogether, the data suggest that whereas glucocorticoids can inhibit both AA generation and corticotropin release, these two effects appear to be causally unrelated.
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PMID:Functional dissociation between glucocorticoid-induced decrease in arachidonic acid release and inhibition of adrenocorticotropic hormone secretion in AtT-20 corticotrophs. 918 58

Previously, we reported that the elevation of plasma noradrenaline and adrenaline induced by intracerebroventricularly (i.c.v.) administered corticotropin-releasing hormone (CRH) was abolished by i.c.v. administered indomethacin, an inhibitor of cyclooxygenase, in rats [Yokotani et al., Eur. J. Pharmacol. 419, 183-189, 2001]. The result suggests the involvement of active metabolites of brain arachidonic acid in the CRH-induced activation of the central sympatho-adrenomedullary outflow. Arachidonic acid is released mainly by two different pathways: phospholipase A2-dependent pathway; phospholipase C- and diacylglycerol lipase-dependent pathway. In the present study, therefore, we tried to identify which pathway is involved in the CRH-induced elevation of plasma catecholamines in urethane-anesthetized rats. CRH (1.5 nmol/animal, i.c.v.)-induced elevation of plasma noradrenaline and adrenaline was abolished by neomycin [0.55 micromol (500 microg)/animal, i.c.v.] and 1-(6-((17beta-3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione (U-73122) [5 nmol (2.3 microg)/animal, i.c.v.] (inhibitors of phospholipase C), and also by 1,6-bis-(cyclohexyloximinocarbonylamino)-hexane (RHC-80267) [1.3 micromol (500 microg)/animal, i.c.v.] (an inhibitor of diacylglycerol lipase). On the other hand, mepacrine [1.1 micromol (500 microg)/animal, i.c.v.] (an inhibitor of phospholipase A2) and 1-(6-((17beta-3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-2,5-pyrrolidinedione (U-73343) [5 nmol (2.3 microg)/animal, i.c.v.] (an inactive analog of U-73122) had no effect. These results suggest that CRH activates the central sympatho-adrenomedullary outflow by the brain phospholipase C- and diacylglycerol lipase-dependent mechanisms in rats.
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PMID:Brain phospholipase C and diacylglycerol lipase are involved in corticotropin-releasing hormone-induced sympatho-adrenomedullary outflow in rats. 1295 58