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

It has been postulated that stress induces discorrelations of the hypothalamo-pituitary and pituitary gonadal axis. In our experiments on the effect of stress on the reproductive physiology in rats and sheep we applied mild electrical footshocking of short or prolonged duration. Foot-shocking applied with some breaks during 9 h within one a day (15th day of the oestrous cycle) induced in ewes acceleration of the release of LH. Prolonged footshocking applied with some breaks during 3 days in cycling sheep caused disturbances in the circadian rhythm of the cortisol secretion, disturbances in the release of LH and led to the blockade of ovulation. Disturbances in the course of oestrous cycle occurred not only during the current cycle but also during two subsequent cycles. Rats exposed to relatively long-term stressful situation (24 h) during dioestrous displayed marked changes in the length of this phase in three subsequent post-stress oestrous cycles. To follow the neurohormonal background of the stress-induced disturbances in LH release and in the course of oestrous cycle in sheep the concentrations of beta-endorphin (beta-END) in the infundibular and paraventricular nuclei as well as in the pituitary gland under physiological and stress conditions were determined, while in rats the metabolism of brain serotonin was investigated. Footshocking in rats induced significant decrease in 5-HT concentrations in the fronto-parietal brain cortex, hippocampus, striatum, medial basal hypothalamus and the preoptic-anterior hypothalamic area. These results allow to suggest that the decline in brain 5-HT under stress conditions has some associations with the impairments in the course of oestrous cycle. Measurements of the beta-END in perfusates of medial basal hypothalamus (nucl. infundibularis) in sheep evidenced significant increase of this opioid under stress conditions and it was postulated that this increase might be the main cause of the stress-induced impairments in the course of oestrous cycle and inhibition of LH-release. In addition, it was found that beta-END suppressed the secretion of cortisol and attenuated some noxious consequences of general nature for organism.
 ...
PMID:Effect of stress on the course of oestrous cycle and the release of luteinizing hormone; the role of endorphin in these processes. 253 47

The aim of this study was to determine whether atrial natriuretic peptide (ANP) alters beta-endorphin (beta-END) secretion from rat intermediate pituitary and whether this effect is a direct action on the intermediate pituitary or an indirect one mediated by hypothalamic factor(s). We studied the release of beta-END from rat neuro-intermediate lobes of the pituitary (NIL) and from the hypothalamo-neurohypophysial complex (HNC), which consists of the hypothalamus, pituitary stalk, intermediate and posterior lobes of the pituitary, by means of an in vitro perifusion system. NIL and HNC were prepared from male Wistar rats and individually perifused for 30 min with perifusion medium followed by 20 min perifusion with medium containing alpha-rat ANP and/or dopamine (DA). Samples of perifusion medium were collected every 5 min and subjected to RIA for beta-END. The basal release of beta-END from NIL was 180% of that from HNC (p less than 0.01), which provides further support for the presence of hypothalamic factors that inhibit beta-END release from the intermediate pituitary. The perifusion of HNC with ANP at 10(-7) and 10(-6) M increased the beta-END concentration by 25 and 50%, respectively (p less than 0.01). In contrast, ANP (10(-8) to 10(-6) M) had no effect on beta-END release from NIL. The inhibitory effect of DA (10(6) M) on beta-END release from NIL and HNC (51% and 50% of the basal release, respectively, p less than 0.01) was confirmed. However, this inhibitory effect was not reversed by ANP.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Effect of atrial natriuretic peptide on the release of beta-endorphin from rat hypothalamo-neurohypophysial complex. 253 54

1. The purpose of this study was to determine the plasma levels of beta-endorphin (beta-END) and ACTH in the perioperative period, define correlations of hormonal plasma levels with clinical parameters and establish the effect of droperidol premedication on hormonal levels and clinical parameters. 2. Twenty two were assigned to one of two groups: (1) Control (no premedication) and (2) droperidol (7.5 mg im) premedication. 3. Venous blood samples and clinical evaluations were done the day prior to surgery, just prior to induction of anesthesia and 1-1.5 hr postoperatively. 4. The results indicate that (1) expectancy of surgery on arrival to the operating room increases beta-END but not ACTH plasma levels, (2) this increase in beta-END is not affected by droperidol administration and (3) postsurgical stress increases beta-END and ACTH above operating room levels. 5. These results indicate that although beta-END and ACTH are both produced by the pituitary and derived from a common precursor, the type of stimuli (pre- versus postsurgical stress) seems to differentially affect their plasma levels.
 ...
PMID:Beta-endorphin and ACTH levels in the perioperative period. 254 52

An endometrial cell line (HRE-H9) was established and characterized to study the mechanism by which gene expression of POMC-derived peptides is controlled in uterine tissues. The HRE-H9 cell line was isolated by transforming primary rabbit endometrial cell cultures, derived from hCG-treated pseudopregnant rabbits, with a temperature-sensitive A209 mutant (tsA209) simian virus 40 at a permissive temperature (33 C). The resulting cells exhibited temperature sensitivity in growth and synthesis of immunoreactive beta-endorphin (ir-beta END). The ir-beta-END present in the cell extracts and culture media was assayed by a specific beta END RIA. Sephadex G-50 gel filtration chromatography of the transformed cell extracts showed three peaks of beta END immunoreactivity. The first peak eluted at the void volume, the second peak coeluted with the beta-lipotropin standard, and the third peak coincided with the porcine beta END standard, ir-beta-END was also detectable in endometrial culture media, suggesting that the transformed endometrial cells secreted POMC-derived peptides. Our data indicate that the tsA209 mutant virus-transformed endometrial cell line provides a suitable model for study of the synthesis and regulation of POMC-derived peptides in extrapituitary tissues.
 ...
PMID:Characterization of a temperature-sensitive beta-endorphin-secreting transformed endometrial cell line. 255 29

In the present study, we present physiological evidence for rate-sensitive, fast feedback inhibition of secretion of ACTH and beta-endorphin (beta END)-related peptides. We used a 2 min restraint stress to physiologically increase plasma corticosterone, then examined the plasma responses of immunoreactive ACTH and beta END plus beta-lipotropin (beta END/beta LPH) to a subsequent restraint stress. After onset of this stress, plasma corticosterone increased from 2.5-10 min at a rate of 120 nM min-1, then remained at a peak from 10-15 min. A single 2 min restraint stress produced peak plasma levels of ACTH and beta END/beta LPH 2.5 min after onset of the stress, and these plasma concentrations declined after this initial stress at rates of 2.7 and 7.4 pM min-1, respectively. Application of a second restraint stress at the time of the peak corticosterone response produced plasma ACTH and beta END/beta LPH responses similar to those after the first stress. Application of a second stress during the period of significant rate-rise of corticosterone in plasma did not result in decreased incremental responses of plasma ACTH or beta END/beta LPH. However, the rates of decline of plasma ACTH and beta END/beta LPH of 7.6 and 32 pM min-1, respectively, from peak levels, were significantly greater after this second stress applied during the period of significant increase in plasma corticosterone concentration than the corresponding rates of decline observed after the initial stress or after a subsequent stress applied at the peak of plasma corticosterone. These differences in rates of decline of plasma ACTH or beta END/beta LPH appear to reflect differences in secretion rate rather than clearance, since disappearance of [125I]ACTH1-24 was not different after an initial vs. subsequent stress. In contrast to these data from intact rats, initial and subsequent stresses did not show different rates of decline of plasma ACTH or beta END/beta LPH in adrenalectomized rats. In conclusion, the stress-induced rate rise of glucocorticoid provides a negative feedback signal which serves to terminate and limit the duration, but not the peak, of the responses of POMC-derived peptides to subsequent stress.
 ...
PMID:Rate-sensitive glucocorticoid feedback inhibition of adrenocorticotropin and beta-endorphin/beta-lipotropin secretion in rats. 255 31

Hypothalamic dopamine neurons are known to control circulating levels of immunoreactive beta-endorphin (i beta-END) by inhibiting hormone secretion by the intermediate lobe (IL) of the pituitary gland. We examined the ability of the D-2 selective dopaminergic agonist, LY141865, to influence circulating levels of i beta-END in rats and found that in contrast to inhibiting IL secretion, LY141865 increased release of i beta-END from the anterior lobe (AL). Intraperitoneal injection of 1 mg/kg LY141865 transiently increased plasma levels of i beta-END by 7-30 min after drug treatment; plasma prolactin levels were maximally reduced within 15 min and throughout the remaining 2-hour time course of treatment. Doses of 0.3 and 1.0 mg/kg of LY141865 increased circulating i beta-END to 440 and 690%, respectively, of control levels (0.38 +/- 0.12 ng/ml, mean +/- SEM, n = 6). Lower doses of the D-2 agonist (0.01-0.1 mg/kg) failed to significantly affect plasma i beta-END. Sephadex G-50 chromatography of plasma pools revealed that virtually all of the increase due to LY141865 treatment was immunoreactivity resembling beta-lipotropin in molecular size, the principal component of AL secretion of i beta-END. Furthermore, LY141865-evoked release was blocked by pretreatment of rats with dexamethasone (50 micrograms/kg i.p., 4 h) which inhibits AL but not IL secretion of pro-opiomelanocortin-derived peptides. Stimulation of i beta-END release by LY141865 was also inhibited by the general dopamine antagonist, haloperidol, (0.1-3.0 mg/kg i.p., 2 h) and by the D-2 selective antagonist, sulpiride (100 micrograms/rat i.c.v., 4 h).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:A D-2 dopaminergic agonist stimulates secretion of anterior pituitary immunoreactive beta-endorphin in rats. 256 71

Culturing sympathetic ganglion neurons in vitro may modify phenotypic expression of some neurotransmitters. For dorsal root ganglia (DRG), contradictory results have been reported; most studies have used immature material. We have therefore performed a detailed immunocytochemical analysis of the transmitter content of cultured adult rat DRG neurons. To demonstrate possible modifications of neurotransmitter phenotypes, we have compared the results obtained with the same techniques on neurons cultured for 3 days and on freshly dissociated DRG cells. Also, the transmitter profile of cultured neurons was compared with that known from in situ studies. Out of 22 antigens studied, 20 were detected in cultured DRG neurons. All of them were expressed in small and/or intermediate-sized cells. Large neurons only contained CGRP, VIP, NPY, beta-END, ENK, and GABA. The percentage of immunostained neurons varied for the various antisera: less than 10% of cultured neurons were positive for ENK, beta-LPH, beta-END, DYN, VASO, and OXY; 10-30% for SOM, CCK, CAT, and SP; and greater than 30% for NPY, CRF, GLU, NT, VIP, GABA, GRP, CGRP, 5-HT, and TRH. In the latter two groups of transmitters (except CGRP), the proportion of immunoreactive neurons was by far larger in cultured than in freshly dissociated DRG. The most pronounced (greater than 25%) increase in the proportion of positively stained neurons after culturing was observed for the GRP, CRF, TRH, and 5-HT antisera. Serotonin was the only transmitter identified in cultured but not in freshly dissociated cells. These data indicate, on one hand, that various antigens, for example, CAT, GABA, NT, TRH, NPY, beta-LPH, and beta-END, which up to now have not been described in DRG in situ, can be detected immunocytochemically a few hours after dissociation of adult rat DRG. On the other hand, several transmitters, for example, VIP, NPY, SP, GABA, GLU, NT, GRP, CRF, TRH, and 5-HT, are expressed in a significantly higher proportion of cells in cultured than in freshly dissociated preparations. This might reflect a change in the phenotypic expression of transmitters due to the new environment generated by the culture conditions, a hypothesis that can be tested by measuring specific mRNA levels. Moreover, considering the plasticity and multipotentiality of their transmitter phenotype, cultured adult DRG neurons might represent an interesting material for autografts into the injured central nervous system.
 ...
PMID:Neurotransmitter phenotype plasticity in cultured dissociated adult rat dorsal root ganglia: an immunocytochemical study. 256 40

Previous studies have indicated that acute stress in vivo or ovine corticotropin releasing hormone (oCRH) in vitro, releases both beta-lipotropin (beta-LPH) and beta-endorphin (beta-END) from the anterior lobe, with beta-END predominating over beta-LPH by 2:1. However, repeated stress shifts this ratio to proportionately more beta-LPH released with re-stress or oCRH in vitro. Alternative hypotheses were that the glucocorticoids released during stress altered the processing of proopiomelanocortin (POMC) or that the increased biosynthetic drive resulted in an inability of the processing enzymes to keep pace with biosynthesis. To distinguish between these alternatives, adrenalectomy studies were performed. Following removal of glucocorticoid negative feedback there is greatly increased secretion of beta-END-IR from anterior lobe corticotrophs with a subsequent increase in biosynthetic drive. Under these conditions of increased biosynthetic drive in the absence of steroids, the corticotroph secretes primarily beta-LPH, suggesting that increased biosynthetic drive alters the posttranslational processing rate of POMC.
 ...
PMID:Adrenalectomy increases beta-lipotropin secretion over beta-endorphin secretion from anterior pituitary corticotrophs. 260 76

Cerebrospinal fluid (CSF) concentrations of beta-endorphin-like immunoreactivity (END-IR) were determined in 11 female and 6 male patients fulfilling the diagnostic criteria of panic disorder (PD) and in matched controls. Eleven of the PD patients had been taking moderate doses of benzodiazepines (BZD) irregularly without satisfactory effect against the panic attacks while six were totally drug-free. No medication was allowed for at least 24 hours before the lumbar puncture. In six patients a second lumbar puncture was performed after 2 to 3 months of treatment with imipramine or clomipramine. In PD patients, CSF levels of END-IR were significantly higher than in controls. Patients that had been taking BZD had somewhat higher concentrations of END-IR than those taking no medication; however, totally drug-free patients also displayed END-IR levels that were significantly higher than in controls. Although they effected a dramatic reduction of the panic attacks, antidepressants did not influence CSF END-IR concentrations.
 ...
PMID:Increased cerebrospinal fluid levels of endorphin immunoreactivity in panic disorder. 278 61

The effect of the opiate peptide, beta-endorphin (beta-END), on the autologous and allogeneic mixed lymphocyte reaction was examined. Physiologic concentrations of beta-END augmented proliferation of the autologous mixed lymphocyte reaction (AMLR) but the allogeneic MLR was not altered. Alpha-endorphin (alpha-END) was ineffective. Pre-incubation of the stimulator subset (i.e., B cells and macrophages) with 10(-8) M beta-END followed by addition to AMLR culture without additional opiate peptide did not produce augmentation. The beta-END-induced augmentation of the AMLR was partially inhibited by the opiate antagonist naloxone. beta-END augmentation was not due to increased secretion of interleukin-2. When prostaglandin E2 (PGE2) was added to AMLR cultures wherein the stimulator cell fraction was vigorously depleted of adherent cells, suppression was observed which could be reversed by the addition of beta-END (10(-8) M). The potential mechanisms producing the increased proliferative response during the AMLR are discussed.
 ...
PMID:Modulation of the autologous mixed lymphocyte reaction by beta-endorphin. 282 56


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>