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)

In the rat, exposure to stress increases prolactin (Prl) secretion, and endogenous opioid peptides (EOP) are believed to play a role in this response. The aim of the present study was to evaluate the specific involvement of the different EOP (i.e. beta-endorphin [beta-END], dynorphin A [DYN-A], methionine-enkephalin [Met-ENK], and/or opiate receptors (i.e., mu/epsilon, kappa, delta) in the stress-related increase in circulating Prl. Rats were subjected to inescapable intermittent footshock (60 Hz, 2.5 mA, 1 s duration, 2 h) 2 h after the intracerebroventricular (i.c.v.) injection of specific antisera raised against beta-END, DYN-A or Met-ENK. In addition, selective opiate antagonists (beta h-END-[6-31], a peptide beta-END antagonist [5 nmol, i.c.v.], beta-funaltrexamine [beta-FNA], an mu 1 receptor antagonist [4.8 nmol, i.c.v.], Mr 1,452 MS and Mr 2,266 BS, two kappa-receptor antagonists [10 mg/kg body weight, i.p.], ICI 154, 129, a delta-receptor antagonist [100 nmol, i.c.v.]) were administered prior to footshock stress. Blood samples were collected through an indwelling jugular cannula. Exposure to footshock rapidly and significantly increased plasma Prl levels. This stress-induced release of Prl was reduced by both antisera against beta-END or DYN-A, as well as by pretreatment with beta h-END-(6-31), beta-FNA and kappa-receptor antagonists. Antiserum against Met-ENK and delta-antagonist were inactive. These results suggest that the activation of the two endogenous opioid systems, beta-END and DYN-A, centrally modulate the release of Prl induced by footshock stress.
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PMID:Beta-endorphin and dynorphin participate in the stress-induced release of prolactin in the rat. 288 85

The influence of alpha-melanocyte stimulating hormone (alpha-MSH) and beta-endorphin (beta-END) on the secretion of somatostatin (SRIF) from the median eminence (ME) was studied using an in vitro incubation system. The MEs from adult male rats were first preincubated at 37 degrees C for 30 min with constant shaking in 0.4 ml of Krebs-Ringer bicarbonate-glucose buffer (pH 7.4) containing bacitracin in an atmosphere of 95% O2/5% CO2. Medium was discarded and replaced by medium containing different doses of alpha-MSH, beta-END, or a fixed dose of alpha-MSH (10(-7) M or 10(-9) M) plus beta-END at various concentrations. By themselves alpha-MSH and beta-END did not alter basal SRIF release, but in the presence of alpha-MSH (10(-7) M) beta-END stimulated somatostatin release. This effect was significant at concentrations of beta-END of 10(-8) M and higher. The permissive effect of alpha-MSH was observed at a concentration as low as 10(-9) M, but in this case the stimulatory effect of beta-END became evident only at higher doses tested (10(-7) M). It is suggested that alpha-MSH and beta-END participate in the modulation of SRIF release. By themselves beta-END and alpha-MSH did not affect basal release of SRIF but in the presence of alpha-MSH, beta-END had a stimulatory effect on SRIF release. The mechanism for this interaction is unknown. The results are consistent with the possibility that beta-END neurons have stimulatory and inhibitory effects on SRIF release and that alpha-MSH, by blocking the inhibitory components, discloses the stimulatory effect of beta-END on SRIF release.
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PMID:Alpha-melanocyte stimulating hormone discloses a stimulatory effect of beta-endorphin on somatostatin release. 288 55

The present study investigates the possible role of endogenous opioid peptides in mediating the inhibitory effect of corticotropin-releasing factor (CRF) on circulating luteinizing hormone (LH). The central injection of an antiserum against beta-endorphin (beta-END) reversed CRF-induced LH decrease in castrated male rats, while antisera raised against DYN-A or M-Enk were inactive. beta-END-(6-31) (2 nmole, icv), a beta-END antagonist, and beta-funaltrexamine (4.8 nmole, icv), a mu 1 opiate receptor antagonist, also reversed the effect of CRF on LH. Either kappa (Mr 1456 and Mr 2266) (10 mg/kg, ip), or delta (ICI 154,129) (10 nmole, icv) opiate receptor antagonists did not significantly modify the inhibitory effect of CRF on circulating LH levels. These results suggest that central beta-END participates in the inhibitory action of CRF on LH secretion.
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PMID:beta-Endorphin modulates the inhibitory action of corticotropin-releasing factor on luteinizing hormone secretion. 289 71

The concentrations of beta-endorphin (beta-END), dynorphin (DYN) and methionine-enkephalin (MEK) in pituitary, brain regions, heart, kidney and adrenal of 8 week old male spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) normotensive rats were determined by radioimmunoassay and compared. The brain regions examined were hypothalamus, striatum, pons + medulla, midbrain and cortex. The concentration of beta-END in pituitary of SHR rats was 49% higher than those of WKY rats. The concentration of beta-END in the striatum of SHR rats was 71% lower as compared to WKY rats. The concentration of beta-END in the heart, adrenals and kidney of SHR rats was significantly lower (92, 48 and 57%, respectively), than those of WKY rat tissues. The concentration of DYN in pituitary, striatum and heart were lower by 38, 55 and 46%, respectively, in SHR compared to WKY rats, but in hypothalamus it was greater (33%) than in WKY rats. The concentration of DYN in other brain areas and in kidney and adrenal did not differ. The tissues of SHR and WKY rats which showed significant difference in the concentration of MEK were pituitary, pons + medulla, cerebral cortex and adrenals. The concentration of MEK was greater in SHR rats with pons + medulla, cortex and adrenals showing 33, 40, 268% higher levels, respectively, over the WKY rat tissues. However, the concentration of MEK in pituitary of SHR rats was 40% lower than that of WKY rats. These studies suggest that the endogenous opioid peptides of both central and peripheral tissues may be important in the regulation of blood pressure in SHR rats.
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PMID:Opioid peptides in pituitary gland, brain regions and peripheral tissues of spontaneously hypertensive and Wistar-Kyoto normotensive rats. 289 47

A study was made of the influence of early exposure to beta-endorphin (beta-END) on the adult behavior and response to beta-END in male rats. beta-END was given during a neonatal period, at 1-5 days of age (1 microgram/animal/day s.c.). Recordings of the development of home-nest-orientation ability, body weights, and sex-specific approach behavior showed that the early beta-END treatment did not have debilitating or other non-specific effects. The early beta-END treatment did cause significant changes in the establishment of the adult pattern of sex-specific approach behavior. Copulatory behavior was not apparently influenced. Intracerebroventricular injection of beta-END (1 microgram) at an adult age induced changes in exploratory and copulatory behaviors and in the pattern of sex-specific approach behavior. The reaction to this treatment with respect to components of socio-sexual behavior differed significantly between males treated early with beta-END and their corresponding controls. No differences were observed in behaviors in the exploratory test situation. It is concluded that early beta-END treatment in rats influences components of socio-sexual behavior and the response to exogenous beta-END in adulthood.
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PMID:Influence of early beta-endorphin treatment on the behavior and reaction to beta-endorphin in the adult male rat. 293 Aug 62

The effect of angiotensin II (A II) on the release of beta-endorphin-like immunoreactivity (beta-END-LI) in rats was studied in vivo and in vitro. Intravenous injection of 1 microgram/100 g body weight of A II resulted in significant increase in the plasma beta-END-LI level after 10 and 20 min. Intraventricular injection of 1 ng/100 g body weight of A II also resulted in significant increase in the plasma beta-END-LI level after 10 min. A II at concentrations of 10(-12) M-10(-10) caused dose-dependent stimulation of beta-END-LI release from dispersed cells of rat anterior pituitary. On gel chromatography, the beta-END-LI released by incubation of the cells with 10(-10) M A II separated into two components which eluted in the same positions as human beta-lipotropin and human beta-endorphin, respectively. The ratio of beta-LPH to beta-END in these fractions was 5:1 on a molar basis. A II did not stimulate beta-END-LI release in Ca++-free-medium. [Sar1, Ala8]-A II at concentrations of 10(-9) M - 10(-7) M did not stimulate beta-END-LI release from the cells. Addition of [Sar1, Ala8]-A II to the incubation medium inhibited A II-induced beta-END-LI release from the cells. These results indicate that A II acts, at least in part, directly on anterior pituitary cells to stimulate beta-END-LI release and that calcium ion is involved in the mechanism of this effect.
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PMID:In vivo and in vitro effects of angiotensin II on the release of beta-endorphin-like immunoreactivity. 293 Dec 75

Long-term treatment of rats with haloperidol, a dopamine receptor antagonist, produced a dose-dependent increase in immunoreactive beta-endorphin (i beta-END) concentrations in the neurointermediate lobe of the pituitary (NIL). In contrast, chronic haloperidol treatment had no significant effect on i beta-END levels in the hypothalamus, the midbrain or in discrete, microdissected brain nuclei even when administered at a dose (5 mg/kg) ten-fold higher than that which elevated i beta-END levels in the NIL. Chronic treatment with bromocriptine, a dopamine receptor agonist, had the opposite effect on the NIL, lowering i beta-END levels to approximately one-third of control values, but it did not affect hypothalamic i beta-END concentrations. These data are consistent with prior evidence that the synthesis of beta-END by IL melanotrophs is reciprocally modulated by dopaminergic ligands. The results indicate, however, that beta-END-releasing neurons are not similarly regulated.
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PMID:Long-term haloperidol treatment elevates beta-endorphin levels in the intermediate pituitary but not in rat brain. 293 16

We have established the content and molecular species of immunoreactive beta-endorphin (ir-beta-END) and immunoreactive N-acetyl-endorphin (ir-Nac-END) in rat neurointermediate lobe by specific radioimmunoassay (RIA) and high-performance liquid chromatography after chronic administration of dopamine (DA) agonists and antagonists. The DA agonist, bromocriptine, reduces tissue levels of all major immunoreactive species, in particular the C-terminally shortened N-acetylated forms. The DA antagonist, haloperidol, proportionally increases all immunoreactive forms, except Nac-beta-END, thus altering the relative abundance of this species. These data indicate that DA is involved in the control of both tissue levels and processing of beta-END-like peptides in the rat neurointermediate lobe.
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PMID:Dopaminergic agents differentially alter beta-endorphin processing patterns in the rat pituitary neurointermediate lobe. 293 29

The concentrations of beta-endorphin like immunoreactivity (beta-END) in the hypothalamus, pituitary and plasma were studied in rats of either sex, one month after induction of diabetes by single iv injection of streptozotocin. As controls, both normal and undernourished rats, weight-matched with diabetic rats, were used. Diabetic male and female rats had a marked depletion of beta-END stores in the hypothalamus and neurointermediate lobe (NIL) but not in the anterior pituitary. Depletion of beta-END was reversed to normal by insulin replacement therapy. Severe undernourishment was not as effective as diabetes to reduce beta-END stores in the hypothalamus and NIL. A significant reduction of beta-END was observed only in the NIL of undernourished female rats. Plasma beta-END and beta-lipotropin (beta-LPH) concentrations were not significantly altered in diabetic rats. These results indicate that the lack of insulin may affect beta-END synthesis in the hypothalamus and NIL.
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PMID:Beta-endorphin concentrations in the hypothalamus, pituitary and plasma of streptozotocin-diabetic rats with and without insulin substitution therapy. 293 94

The role that opiate peptides play in suckling-induced prolactin (PRL) release was examined in 10-day postpartum lactating rats. The opiate receptor antagonist naloxone (NAL) suppressed suckling-induced PRL release in a dose-dependent manner and a large dose abolished the response. These results suggest either that opiate neurons are situated in the neuronal pathway mediating this neuroendocrine response, or alternatively, that opiate neurons are situated such that they can modulate neuronal transmission in this pathway. It is suggested that NAL blocks a tonic, inhibitory beta-endorphinergic input to the tuberoinfundibular dopaminergic (TIDA) neurons, hence, NAL administration in effect stimulates the TIDA neurons and in this way overrides the suckling response. Intravenous, bolus administration of beta-endorphin (beta-END) produced a PRL response that was similar to the suckling response in terms of latency of onset and duration while the magnitude of the beta-END-induced response was 2-fold greater than that produced by the suckling stimulus. NAL abolished beta-END-induced PRL release at a much lower dose than that required to inhibit suckling-induced PRL release. This suggests that the neural mediation of the suckling response involves a mechanism in addition to the one inhibited by opiate receptor blockade.
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PMID:Suckling-induced prolactin release is suppressed by naloxone and simulated by beta-endorphin. 293 73


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