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 vivo single-unit extracellular recording was used to assess neuronal membrane sensitivity at the level of the midbrain central gray (MCG) to the iontophoresis of luteinizing hormone releasing hormone (LHRH) and beta-endorphin (beta-END). The percentage of change in firing rate was evaluated to determine the effect of exogenously administered estradiol benzoate (EB) and EB plus progesterone (EB + P) on the membrane sensitivity of these MCG neurons to LHRH and beta-END. Ovariectomized adult female rats were primed with EB or EB + P, or nonprimed, 24-48 h prior to recording. EB priming significantly altered the membrane sensitivity of neurons in the MCG to LHRH by increasing the number of cells excited compared to the EB + P group and the nonprimed controls (p less than 0.005). The addition of P appeared to negate this effect. Hormonal priming did not alter the response profile for beta-END iontophoresis. The results suggest an estrogen-dependent sensitivity to LHRH at the MCG which translates into an increased electrical output, ultimately facilitating lordosis behavior. P treatment dampens this excitation. beta-END's effect on neuronal membrane excitability at the MCG was not distinctly characterized under the hormonal conditions our study evaluated and may reflect a regulatory role under physiological extremes.
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PMID:Estrogen priming affects the sensitivity of midbrain central gray neurons to microiontophoretically applied LHRH but not beta-endorphin. 295 30

Levels of beta-endorphin-like immunoreactivity (beta END-LI) in uterine secretions were studied in pseudopregnant and ovariectomized gilts treated with ovarian steroids. Pseudopregnancy was induced in 7 gilts by daily injection of estradiol valerate (5 mg/day) between days 11 and 15 of the estrous cycle. Between days 60 and 90 of pseudopregnancy, uterine secretions were collected by flushing the uterus with 0.9% saline. Uterine flushings were extracted with a Sep-Pak C-18 column and assayed for beta END-LI by a specific RIA. The RIA cross-reacted only with beta-lipotropin (15%). Significant amounts of total immunoreactive beta END-LI were detected in the uterine flushings. The inhibition curve for extracts was parallel to the standard END inhibition curve. Extracted uterine flushings were applied to a Sephadex G-50 column. Three peaks of immunoreactive beta END-LI were detected. One peak eluted at the void volume. The second peak eluted at a Kav of 0.21, which was near the Kav of a lipotropin standard (0.23). The highest peak (Kav = 0.53) eluted similar to standard END (Kav = 0.51). In the second experiment, 12 gilts were ovariectomized on day 4 of the estrous cycle and randomly assigned to 4 groups of 3 gilts each. Each group received 1 of the following daily injections: vehicle (corn oil), 0.1 mg 17 beta-estradiol (E2), 200 mg progesterone (Prog), or a combination of E2 and Prog (E2 + Prog). After treatment for 30 days, beginning on the day of ovariectomy, the uterine flushings were assayed for beta END-LI and total protein. Treatment with Prog increased (P less than 0.05) total beta END-LI 532% (12.4 ng) compared to corn oil treatment (2.3 ng), and levels were significantly higher than with E2 (2.9 ng) or E2 + Prog treatment (5.1 ng). Opiate receptor assay showed that extracts of uterine flushing had a displacement curve parallel to that of standard porcine beta END. Results suggest that significant amounts of immunoreactive beta END-LI are present in uterine secretions of gilts and that the accumulation of beta END-LI is influenced by ovarian steroids.
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PMID:Beta-endorphin in uterine secretions of pseudopregnant and ovariectomized, ovarian steroid-treated gilts. 295 91

The present study examines whether sustained changes in the biosynthetic activity of the intermediate pituitary, induced pharmacologically by treating rats with dopamine receptor ligands, alters the post-translational processing of beta-endorphin (beta-END). Separation of the individual molecular forms of beta-END using ion exchange chromatography revealed that beta-END is processed to alpha-N-acetylated and nonacetylated forms of beta-END-(1-31), beta-END-(1-27) and beta-END-(1-26) in the neurointermediate lobe (NIL). Chronic treatment with D-2, but not D-1, dopamine receptor antagonists elevated total beta-END immunoreactivity (i beta-END) in the NIL but this increase was predominantly attributable to elevations in the concentrations of N-acetyl-beta-END-(1-31) and N-acetyl-beta-END-(1-27). In contrast, N-acetyl-beta-END-(1-26) was not significantly affected. The dopaminergic agonist, bromocriptine, had the opposite effect; it lowered total i beta-END levels, depleting N-acetyl-beta-END-(1-31) and N-acetyl-beta-END-(1-27) to a greater extent than N-acetyl-beta-END-(1-26). beta-END peptides were released in vitro in the same relative proportion as they were contained in the NIL suggesting that individual molecular forms of beta-END are not released preferentially. i gamma-END levels also were modulated by dopaminergic agents but the processing of gamma-END and alpha-END was not altered. Acute haloperidol treatment depleted i gamma-END levels but did not affect the pattern of beta-END peptides in the NIL. These results indicate that dopaminergic agents influence not only the secretion but also the post-translational processing of pituitary beta-END.
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PMID:Dopaminergic agents selectively alter the post-translational processing of beta-endorphin in the intermediate pituitary of the rat. 295 68

The effects of subcutaneous (s.c.) administration of compound 48/80 (a well known histamine liberator) on latency to thermoalgesic stimulus, hematocrit (Hct) and plasma levels of beta-endorphin-like immunoreactivity (beta-END-LI) were investigated in male rats. The s.c. administration of compound 48/80 in doses ranging from 0.5 to 5.0 mg/kg into the rats produced significant analgesia in the hot plate test and increased Hct in a dose-dependent manner. Concomitant variation was observed between the analgesia and the increase of Hct. This analgesic effect, but not the increase of Hct, was diminished by pretreatment with the opiate receptor antagonist, naloxone (5 mg/kg, s.c.). A significant increase of plasma beta-END-LI was observed by s.c. injection of compound 48/80. Together with a previous finding that compound 48/80 induced-hypovolemia increases the renin release from kidney and then causes water intake in the rats, it is suggested that s.c. administration of compound 48/80 induced analgesia mediated through stimulation of an opioid system, may be closely related to stimulation of the renin-angiotensin system.
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PMID:Analgesia and plasma beta-endorphin-like immunoactivity in compound 48/80-induced hypovolemia of the rats. 296 94

The effects of bile salts on the release of beta-endorphin-like immunoreactivity (beta-END-LI) were investigated in men using a specific radioimmunoassay developed by the authors. Plasma beta-END-LI was determined after extraction by the acid-acetone method (recovery: 73 +/- 5%). Oral administration of 400 mg of sodium taurocholate caused a rise in plasma beta-END-LI from 9.9 +/- 0.5 pmol/liter to 21.3 +/- 1.2 pmol/liter after 30 min and 18.1 +/- 0.5 pmol/liter after 60 min, with return to the initial value after 90 min. Oral administration of chenodeoxycholic acid (CDCA) also increased plasma beta-END-LI from a basal level of 8.4 +/- 0.7 pmol/liter to 18.7 +/- 0.8 pmol/liter after 30 min. Oral administration of ursodeoxycholic acid (UDCA) increased plasma beta-END-LI from 7.3 +/- 0.3 pmol/liter to 30.6 +/- 0.2 pmol/liter after 30 min. In gel chromatography, the beta-END-LI released after UDCA administration separated into two components, which eluted in the same positions as human beta-lipotropin and human beta-endorphin, respectively. These results suggested that bile salts may participate the release of beta-END-LI.
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PMID:Effects of bile salts on plasma concentration of beta-endorphin-like immunoreactivity in men. 296 67

This paper further substantiates the physiological role of beta-endorphin (beta-END) in the control of the cyclic LH secretion and provides new data on the interactions between 17 beta-estradiol (17 beta-E2) and beta-END at both the hypothalamic and pituitary levels. At the hypothalamic level, during the estrous cycle in rats, beta-END concentrations were highest on diestrus I in the arcuate nucleus, median preoptic area and median eminence and lowest at the time of the preovulatory 17 beta-E2 surge on proestrus, before the subsequent preovulatory hypothalamic GnRH and plasma LH surges. Data obtained in ovariectomized 17 beta-E2-treated ewes support the direct involvement of 17 beta-E2 in changes in beta-END and GnRH concentrations in these hypothalamic areas. At the anterior pituitary level, in vitro results obtained using anterior pituitaries from the proestrus morning cycling female rat have shown that 17 beta-E2 strongly suppresses beta-END secretion and that GnRH stimulates the release of beta-END. Furthermore, marked fluctuations were observed for plasma beta-END throughout the menstrual cycle in the woman. Low beta-END concentrations were observed in the period preceding the LH preovulatory surge. Taken together, these results show that: (1) decreases in hypothalamic beta-END concentrations, which are controlled at least by circulating levels of 17 beta-E2, modulate GnRH synthesis and/or release and contribute to the mechanisms which initiate the LH surge; (2) anterior pituitary beta-END might be involved in the mechanisms which terminate the LH surge.
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PMID:Interactions between 17 beta-estradiol and the hypothalamo-pituitary beta-endorphin system in the regulation of the cyclic LH secretion. 296 83

An in vitro perifusion system was used to characterize spontaneous immunoreactive beta-endorphin (i beta-END) release from 10 human fetal (20-23 weeks gestation) and 2 human adult anterior pituitaries. Spontaneous i beta-END release from fetal anterior pituitaries was pulsatile, with a mean (+/- SE) pulse interval of 9.1 +/- 0.5 minutes, pulse amplitude of 120.8 +/- 46.1 pg with nadir to peak increment of 106.0 +/- 32.9%, and overall release rate of 209.7 +/- 65.0 pg/2 minutes. Blockade of calcium activity with 10 microM verapamil and 4 mM EGTA suppressed the frequency and amplitude of the spontaneous pulsatile i beta-endorphin release (n = 2). Administration of 2 nM human CRF for 20 minutes at the end of 2 perfusions induced 205 and 883% increases of i beta-END release over the preceding basal levels. Administration of 2 nM CRF for 50 minutes at the end of another perifusion led to a greater and prolonged increase (maximum 4620% relative to the immediately preceding basal level) in i beta-END release. Addition of 56 mM KCl during the last 20 minutes of this prolonged CRF stimulation further increased i beta-END release (to 7680% relative to the baseline preceding the CRF stimulation). Each of 4 quarters of adult anterior pituitaries (2 quarters each from 1 male and 1 female) also released i beta-END in a pulsatile fashion, with a pulse interval of 11.8 +/- 2.0 minutes, pulse amplitude of 7.4 +/- 0.8 ng with nadir to peak increment of 51.4 +/- 15.3%, and overall release rate of 21.7 +/- 2.9 ng/2 minutes. These studies demonstrate that i beta-END release from the isolated human anterior pituitary in vitro is characterized by high-frequency pulses, independent of hypothalamic stimulation. This spontaneous calcium-dependent pulsatile i beta-END release apparently reflects the activity of an intrapituitary pulse-generating mechanism.
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PMID:Pulsatile beta-endorphin release from the human pituitary in vitro. 297 72

We have recently shown that the posterior pituitary (neurointermediate lobe) contains a potent prolactin (PRL)-releasing factor (PRF) which is distinct from known PRL secretagogues. Posterior pituitary PRF appears to be a small peptide of an unknown cellular origin. Using pituitary stalk-sectioned (SS) male rats, the objectives of this study were: (1) to determine if PRF is transported from the hypothalamus or is synthesized within the pituitary gland, and (2) to compare changes in PRF activity with alterations in the posterior pituitary content of beta-endorphin (beta-END), oxytocin (OXY), and dopamine (DA). One or two weeks following pituitary SS or sham surgery (SHAM), acid extracts of the posterior pituitary and medial basal hypothalamus (MBH) were analyzed for their hormone content. PRF activity was assessed by determining the stimulation of PRL secretion from perifused anterior pituitary cells, DA was measured by HPLC, and OXY and beta-END levels were determined by RIAs. OXY and DA concentrations in the posterior pituitary were reduced more than 95% at both 1 and 2 weeks after SS. PRF activity in the posterior pituitary was significantly reduced by 75 and 90%, 1 and 2 weeks after SS, respectively. In contrast, beta-END levels in the posterior pituitary at these times increased 20 and 60%, as compared to SHAM rats. Unlike the posterior pituitary, OXY levels in the MBH increased 123% 1 week following SS, and 1,260% at 2 weeks. These increases may reflect the accumulation of OXY-containing secretory vesicles in the severed nerves. DA concentrations in the MBH showed a biphasic pattern. DA levels were initially decreased by 70%, and then increased, but remained 30% below SHAM levels. The reason for these alterations in DA levels is not clear.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential effects of pituitary stalk-section on posterior pituitary and hypothalamic contents of prolactin-releasing factor, oxytocin, dopamine and beta-endorphin. 297 37

Four experiments were conducted to evaluate the effect of beta-endorphin (beta-END) on feeding, drinking and colonic temperature in rapidly growing (Rock-Cornish; RC) and slow growing (Single-Comb White Leghorn; SCWL) stocks of chickens. In the first experiment RC cockerels were injected intracerebroventricularly (ICV) with 0, 1.5, 3.0 and 6.0 micrograms of beta-END. In the second experiment RC cockerels were injected ICV with 0.5, 1.0 and 2.0 micrograms of beta-END. Experiments 3 and 4 were conducted identically to Experiment 1 and 2, respectively, except SCWL were used. Administration of beta-END at levels between 1.5 and 6.0 micrograms produced a significant curvilinear increase in feeding in both RC and SCWL chicks. In RC chicks, feeding was significantly elevated at 45 min and from 90 through 240 min postinjection, whereas in SCWL chicks feeding was increased from 90 through 300 min postinjection. Water intake was depressed in RC and SCWL from 60 through 90 min and from 30 through 60 min postinjection, respectively. Significant increases in water occurred at 180 and 300 min postinjection in SCWL. beta-END also induced a significant hyperthermia in RC and SCWL from 30 through 240 min and from 15 through 180 min postinjection, respectively. At low levels of beta-END, i.e., 0, 0.5, 1.0 and 2.0 micrograms, feeding, drinking and body temperature were significantly increased in both stocks. Feeding in RC chicks was stimulated in a linear fashion from 180 through 300 postinjection while feeding in SCWL was stimulated in a curvilinear manner from 180 through 240 min postinjection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Feeding, drinking and temperature responses to intracerebroventricular beta-endorphin in the domestic fowl. 297 59

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


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