UNIPROT:P01189 - FACTA Search

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Query: UNIPROT:P01189 (beta-endorphin)
21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of intracerebroventricularly (i.c.v.) injected interleukin-1 beta (IL-1 beta: 1, 2.5, 10, and 25 ng) were studied on plasma growth hormone (GH) and prolactin (PRL) concentrations in freely moving rats chronically implanted with i.c.v. cannulas and intracardial catheters. Significant changes in PRL secretion were not found. Small i.c.v. doses of IL-1 stimulated GH secretion 15 min postinjection (significant after 2.5 ng IL-1) whereas high doses of IL-1 suppressed plasma GH concentrations. The stimulation of GH secretion by 2.5 ng IL-1 was abolished when endogenous growth hormone-releasing hormone (GHRH) was immunoneutralized by pretreating the rats with GHRH antibodies. The results indicate that IL-1 elicits GH secretion by stimulating the release of hypothalamic GHRH. The inhibition of GH secretion after high doses of IL-1 is attributed to the previously reported corticotropin-releasing-hormone-releasing activity of IL-1.
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PMID:Stimulation and inhibition of growth hormone secretion by interleukin-1 beta: the involvement of growth hormone-releasing hormone. 164 Oct 70

The effects of 2 weeks of lithium carbonate administration at therapeutic plasma levels were examined in 11 normal volunteers. Serotoninergic function before and after lithium administration was assessed using low-dose intravenous clomipramine hydrochloride challenge, while urinary and plasma metabolites of norepinephrine (NE) were used to assess noradrenergic systems. Long-term lithium administration in normal subjects did not significantly or consistently enhance serotonin-mediated neuroendocrine responses but did increase measures related to neuronal release of NE. No statistically significant effects of lithium on prolactin, corticotropin, or cortisol responses to serotoninergic challenge could be detected. The probability of a type II error was assessed, and a doubling of prolactin level was unlikely to have been missed, although more modest increases (less than 75%) could have been overlooked. After 2 weeks of lithium administration, there were significant increases in 24-hour urinary excretion of NE, normetanephrine, and fractional NE release, compatible with increased neuronal release of NE and a lithium-induced subsensitivity in alpha 2-adrenergic receptor function. These changes were not statistically significant after 1 week of administration, suggesting that increased NE release is characteristic of long- rather than short-term lithium administration. Since previous reports have demonstrated enhanced prolactin responses after short- but not long-term lithium use, the present study points to temporal specificity in lithium's effects on both serotoninergic and noradrenergic function. Lithium's effects on NE release were consistent but small (a 16% increase), while its effects on serotoninergic responses were larger (a 50% increase in prolactin responses) but quite inconsistent, suggesting that neither of these systems is the primary site of action of lithium.
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PMID:The mechanisms of action of lithium. I. Effects on serotoninergic and noradrenergic systems in normal subjects. 842 26

Many behavioral responses to cocaine become progressively exaggerated with chronic treatment. Most studies have focused on cocaine-induced locomotor stimulation and changes in the dopamine projection systems which mediate these actions. However, it is not clear if a uniform 'sensitization' develops in all dopamine systems during chronic stimulant administration. To test this possibility the neuroendocrine actions of cocaine which are mediated, in part, by hypothalamic dopamine neurons were evaluated after chronic cocaine administration. Treatment of rats with cocaine (15 mg/kg, 2x/day) markedly enhanced the locomotor response to cocaine after 3 and 7 days of chronic administration. In contrast, neither the stimulation of adrenocorticotropic hormone (ACTH)/corticosterone (CS) secretion nor the slight inhibition of prolactin caused by acute cocaine administration changed, although a small elevation of basal corticosterone secretion was observed after 7 days. These findings suggest that the marked sensitization observed in other dopamine systems does not occur in the hypothalamic dopamine neurons thought to mediate the neuroendocrine responses to cocaine during chronic administration, despite recently described commonalities in uptake and autoreceptor functions in these dopamine cell populations. This contrast suggests a role for long loop feedback systems unique to telencephalic dopamine systems or region-specific neurochemical adaptations in cocaine sensitization.
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PMID:Chronic cocaine administration sensitizes behavioral but not neuroendocrine responses. 164 34

From preclimacteric women (n = 10, 45-50 years of age) with gross cystic breast disease, levels of beta-endorphin, estradiol, progesterone, luteinizing hormone, follicle-stimulating hormone, thyroid-stimulating hormone, cortisol and prolactin were assayed radiochemically in the breast cyst fluid and in plasma. The beta-endorphin concentration (fmol/ml) was increased more than fourfold in the breast cyst fluid (17.6 +/- 4.6 SEM) than in plasma (4.2 +/- 0.5 SEM). In the breast cyst fluid, estradiol was increased 41-fold (1738.2 +/- 350.5 SEM pg/ml), and progesterone 47-fold (65.47 +/- 8.25 SEM ng/ml) more than in plasma. The significantly increased values of beta-endorphin, estradiol and progesterone in the breast cyst fluid and the identification of beta-endorphin in cyst-lining epithelia demonstrate the local synthesis. Growth factor-like properties of beta-endorphin and estradiol are accountable for the propagation of cystic changes. The autonomic formation and function of beta-endorphin, estradiol and progesterone in cyst compartments can not be related with the levels of luteinizing hormone, follicle-stimulating hormone, thyroid-stimulating hormone and cortisol, which were significantly higher in plasma than in the breast cyst fluid. In the breast cyst fluid, prolactin could not detected to be significantly higher than in plasma. In addition the plasma-concentration of testosterone, androstenedione, thyroxin, triiodothyronine, thyroid-binding globulin, sexual-hormone-binding-globulin could be detected within the normal range. In this study we could demonstrate the synergism of beta-endorphin, steroid hormones and peptide hormones which advance the growth of gross cystic disease of preclimacteric women. Beta-endorphin was also examined by immunocytochemical assays (fluorescence, alkaline phosphatase and horseradish peroxidase method), in 11 women with pure fibrocystic disease, in 7 women with fibrocystic disease combined with a carcinoma in situ and in 15 women with fibrocystic disease combined with invasive carcinoma of the breast. Sections of frozen and paraffin embedded tissue of the same patient were reacted with anti-beta-endorphin antiserum. The immunoreactivity of beta-endorphin was intense in normal, proliferative altered and cyst-lining epithelia of fibrocystic disease and decreased in atypical epithelia and carcinoma cells of the breast. The degree of beta-endorphin staining is related to the degree of cell differentiation. In addition, nuclear receptors for estrogen and progesterone were assayed by peroxidase antiperoxidase technique.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Interaction between beta-endorphin, steroids and peptide hormones in fibrocystic lesions of the female breast]. 164 46

The present study reports adrenocorticotropic hormone (ACTH) and prolactin responses after oral administration of 0.25 mg/kg of the serotonin agonist, meta-chlorophenylpiperazine (MCPP), in patients with panic disorder (PD) and in healthy subjects. MCPP blood levels were similar for the two groups, but almost twice as high in males as in females. Female patients had augmented ACTH and prolactin release as compared to healthy females, while ACTH and prolactin release in male patients was similar to that of male controls. These results suggest that female PD patients have hypersensitive serotonin receptors. Moreover, they indicate that pharmacokinetic gender differences may affect challenge studies, and that different doses may be required to study neuroendocrine responses in males and females.
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PMID:Pituitary hormone responses to meta-chlorophenylpiperazine in panic disorder and healthy control subjects. 165 Apr 87

The concentrations of beta-endorphin have been shown to change in the rat brain during pregnancy and lactation. This study has been performed in order to analyze whether also brain opioid receptors might undergo significant modifications during these two physiological situations. The maximal binding capacity (Bmax) and the constant of affinity (Ka) of the mu-subpopulation of opioid receptors have been evaluated in the hypothalami of female rats at different stages of pregnancy (7, 15 and 22 days), on the day of parturition (12-18 h after delivery) and 6-8 days postpartum (both in lactating and in nonlactating animals). Female rats killed on the day of estrus served as controls. The receptor binding assay has been performed utilizing [3H]-dihydromorphine [( 3H]-DHM) as the ligand for the mu-opioid receptors. Hypothalamic concentrations of beta-endorphin as well as serum levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH) and prolactin have also been evaluated by radioimmunoassay. The results showed that the concentration of hypothalamic mu-opioid receptors increased during pregnancy, being significantly higher than in the controls at days 15 and 22 of gestation. After delivery, the concentration of these receptors returned towards control values, regardless on whether the animals were lactating or not. The Ka values of [3H]-DHM for the mu-receptors did not change significantly in the different groups of experimental animals. Hypothalamic beta-endorphin content showed a modest though not significant increase at the end of gestation (day 22) and returned to control values 12-18 h after delivery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypothalamic opiatergic tone during pregnancy, parturition and lactation in the rat. 165 58

To study the role of corticotropin-releasing hormone (CRH) in the circadian rhythm of circulating corticotropin (ACTH), beta-endorphin (beta-END), corticosterone, and prolactin (PRL), we measured the effects of CRH immunoneutralization over a 24-hour period in chronically cannulated, conscious, freely moving, male Sprague-Dawley rats, maintained at a constant light-dark cycle. Blood samples were collected in the morning (08.00 h), at noon (12.00 h), and in the evening (18.00 h) on the day of treatment, and in the morning (08.00 h) of the next day. Hyperimmune rabbit serum raised against rat CRH (1.0 ml/rat, i.v.) or normal rabbit serum (NRS, 1.0 ml/rat, i.v.) was administered at 08.00 h, immediately after the first blood sample had been collected. CRH immunoneutralization caused no significant decreases in circulating immunoreactive ACTH, beta-END and corticosterone plasma levels at noon, but abolished the evening rises of these hormones. PRL levels were not significantly different between the groups at any time point measured. To compare the effects of CRH immunoneutralization to those of glucocorticoid negative feedback, we measured the effects of dexamethasone (0.5 mg/kg, i.v. at 08.00 h) on the above parameters. ACTH and beta-END concentrations were significantly decreased, and corticosterone and PRL levels were markedly suppressed after glucocorticoid administration both at 12.00 and 18.00 h. However, 24 h after the administration of dexamethasone, PRL concentrations were elevated despite persistently low corticosterone levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Circadian patterns of plasma immunoreactive corticotropin, beta-endorphin, corticosterone and prolactin after immunoneutralization of corticotropin-releasing hormone. 165 9

To study putative differences in central neurotransmitter function in depressive subtypes, growth hormone, adrenocorticotropic hormone (ACTH), cortisol, and prolactin responses to the alpha 2-noradrenergic receptor agonist clonidine (1.3 micrograms/kg i.v.) were examined in 26 subjects with major depression, 13 of whom had melancholia. The responses of 10 of these endogenous/melancholic subjects were compared with those of 10 controls who were matched to the patients on age, sex, and menopausal status. In 15 of the depressed subjects, prolactin and cortisol responses to the putative serotonergic agonist fenfluramine were also examined to test for associations between these challenges. There were no significant differences in any of the responses between melancholic and nonmelancholic depressive subgroups after controlling for age and sex. With the exception of a greater reduction in ACTH in the endogenous/melancholic subjects, there were also no significant differences in hormonal responses between these patients and controls. There was, however, a significantly greater reduction in systolic blood pressure in the control subjects. There were no significant correlations between the responses to clonidine and fenfluramine. The findings suggest that clonidine at a dosage of 1.3 micrograms/kg is neither able to differentiate reliably between depressive subtypes nor to differentiate reliably between depressed and control subjects.
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PMID:Growth hormone and other hormonal responses to clonidine in melancholic and nonmelancholic depressed subjects and controls. 165 41

Adrenocorticotropic hormone (ACTH), cortisol, and prolactin responses following maximal and submaximal (40 min at 80% maximal O2 consumption) running were studied in eumenorrheic (ER; n = 8, 29.0 +/- 1.5 yr) and amenorrheic (AR; n = 8, 24.5 +/- 2.0 yr) runners. ER were studied in the early follicular and midluteal phases of the menstrual cycle. Physical, training, and gynecological characteristics were similar, and cardiorespiratory and metabolic responses to the exercises were indistinguishable in the groups. ACTH, cortisol, and prolactin data from the follicular luteal phases in ER were combined for comparison to AR, because no differences were noted between the menstrual phases at rest. Similar preexercise ACTH levels and responses following exercise occurred in both groups, but preexercise cortisol levels were elevated (ER = 293.1 +/- 46.3, AR = 479.6 +/- 42.4 nmol/l) and cortisol responses blunted in AR. Adrenal sensitivity was blunted in AR compared with ER after submaximal (ER = 121.9 +/- 17.4, AR = 51.7 +/- 13.6) and maximal exercise (ER = 27.9 +/- 9.2, AR = 12.1 +/- 3.8). Preexercise prolactin levels were reduced (ER = 16.4 +/- 2.7, AR = 10 +/- 2.3 micrograms/l), and prolactin responses to maximal exercises were blunted in AR, despite high lactate levels (11.4 +/- 0.4 mmol/l). We conclude that 1) control for menstrual phase in ER is important in studies of prolactin responses following exercise but not in studies of ACTH and cortisol responses following exercise, 2) cortisol responses following submaximal and maximal exercise in AR are blunted at the adrenal level, 3) prolactin responses following submaximal and maximal exercise are also blunted in AR, and 4) prolactin responses following exercise may be mediated by adrenal activation.
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PMID:Adrenal activation and the prolactin response to exercise in eumenorrheic and amenorrheic runners. 165 6

Phencyclidine (PCP) has been found to affect neuroendocrine function by altering the release of the anterior pituitary hormones, adrenocorticotrophin, luteinizing hormone and prolactin. The purpose of this study was to examine the effect of PCP on release of the two pituitary hormones also derived from the adrenocorticotropin precursor, namely, alpha-melanocyte-stimulating hormone and beta-endorphin (beta-E), synthesized in the neurointermediate and anterior lobes of the pituitary. At behaviorally active doses, PCP administered i.c.v. increased plasma levels of immunoreactive beta-E (i beta-E) without affecting the concentration of immunoreactive alpha-melanocyte-stimulating hormone, suggesting that PCP increased the release of beta-E from only the anterior lobe of the pituitary. Dexamethasone pretreatment blocked the PCP-induced increase in i beta-E which indicated further the anterior lobe effects of PCP. MK-801 [(+)-5-methyl-10,11-dihydro-5H-dibenzo [a,d]cyclohepten-5,10-imine maleate), a selective PCP ligand, at behaviorally active doses also increased the plasma concentration of i beta-E. The dose-response curves for induction of behavior was very different from that for increasing the concentration of i beta-E in plasma. The increase in release of i beta-E was stereoselective as (+)-(1-(1-phenylcyclohexyl)-3 methylpiperidine but not (-)-(1-(1-phenylcyclohexyl)-3 methylpiperidine increased release of i beta-E. The increase in plasma levels of beta-E was not due to an interaction with opioid receptors because naloxone did not block PCP-induced release of beta-E. In vitro, PCP also significantly increased release of i beta-E from anterior lobe of the pituitary.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Phencyclidine increased release of beta-endorphin from anterior lobe of the pituitary. 165 42

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