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)

The neuroendocrine polypeptide hormone beta-endorphin (beta-END), which is released from various tissues including the anterior pituitary gland and cells of the immune system, has recently been implicated as having an immunoregulatory role. We used a radioimmunoassay to measure beta-END levels in circulating mononuclear leucocytes from normal subjects and patients with various rheumatic diseases. Levels of beta-END in leucocytes from patients were lower than in leucocytes from healthy subjects (P less than 0.001). Whereas levels of beta-END in leucocytes from patients with the various rheumatic disorders were not significantly different, an inverse correlation was found between beta-END levels in leucocytes and expression of rheumatoid factor (P less than 0.025) and erythrocyte sedimentation rate (P less than 0.025). This study demonstrates decreased content of beta-END in cells of the immune system related to parameters of inflammatory activity in rheumatic diseases.
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PMID:Decreased immunoreactive beta-endorphin in mononuclear leucocytes from patients with rheumatic diseases. 173 81

A comparison was made of beta-endorphin (B-END) concentrations versus post-translation products during the perinatal period in the hypothalamus and the caudal medulla oblongata. The concentration of B-END-like immunoreactivity did not differ statistically between embryonic day 21 (E21) and postnatal day 1 (P1) in either area. There were significant differences in forms, with a shift from larger precursors at E21 to smaller peptides at P1, with the predominant form of B-END being the 31 residue form at E21 in both regions. B-END varied between the two regions at P1, the 27-26 residue predominant in the hypothalamus, and the 31 residue in the caudal medulla.
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PMID:Characterization of beta-endorphin-related peptides in the caudal medulla oblongata and hypothalamus of the prenatal, postnatal and adult rat. 176 Aug 65

Recent in vitro studies have shown that the release of hypothalamic beta-endorphin (beta-END), like that of adenohypophysial origin, is enhanced by both corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP). However, whereas AVP merely synergizes with CRH in the pituitary, it seems to be essential for the release of hypothalamic beta-END by CRH. The present paper reports on the effects of long-term adrenalectomy (ADX) and subsequent replacement with supraphysiological doses of corticosterone (compound B, CB) upon the in vitro basal and CRH- and AVP-stimulated release of beta-END from the rat hypothalamus. Basal release of beta-END was significantly elevated by ADX, and returned to control levels following CB overdosage. Both ADX and CB replacement significantly reduced the stimulatory effect of CRH (10(-8) M) upon beta-END release. ADX caused no significant change in the AVP (10(-6) M)-induced release of beta-END. However, the AVP-stimulated release of beta-END was completely abolished in ADX rats treated with a high dose of CB. The hypothalamic content of beta-END was also measured following ADX and subsequent CB treatment. Compared with control tissues, those from ADX animals had significantly greater contents of beta-END; the hypothalami from rats with experimentally induced hypercorticalism had markedly reduced concentrations of the opioid peptide. Measurements of basal release and content of AVP in the hypothalamus following long-term ADX and CB treatment revealed that AVP neuronal activity is also subject to manipulations of the glucocorticoid hormone environment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adrenalectomy and experimental hypercorticalism modulate the basal, corticotropin-releasing-hormone- and arginine-vasopressin-stimulated release of hypothalamic beta-endorphin. 176 48

The relationships between the release of LHRH, beta-endorphin (beta-END) and noradrenaline (NA) from the hypothalamic infundibular nuclei/median eminence (NI/ME) during the periovulatory period in the ewe was studied. Neurohormone release was assayed in perfusates collected from the NI/ME via push-pull cannulae. LHRH concentrations in perfusates ranged from below detectable values (5 pg) to 50 pg and from 15 to 240 pg/20 min perfusate on the days of proestrus and estrus, respectively. beta-END concentrations in perfusates ranged from 320 to 6,000 pg on the day of proestrus and fell to a range between 100 and 380 pg/20 min perfusate on the day of estrus. The NA content of perfusates ranged from an undetectable level to 0.9 x 10(4) pg/perfusate during proestrus, and rose from 1.0 x 10(4) to 6.6 x 10(4) pg/perfusate shortly before the preovulatory release of LHRH and LH. On the basis of the present observations, the following sequence of events leading to the massive LH ovulatory surge in the sheep is suggested: (1) increased secretion of beta-END in the NI/ME on the day of proestrus generates an increase in the releasable pool of LHRH through inhibition of LHRH release; (2) on the day of estrus a decreased release of beta-END allows the expression of NA activity in the NI/ME and the augmentation of NA tone facilitates the release of newly accumulated LHRH; (3) the resultant intensified LHRH output with its significantly changing pattern of release triggers the preovulatory surge of LH.
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PMID:Release of luteinizing hormone-releasing hormone, beta-endorphin and noradrenaline by the nucleus infundibularis/median eminence during periovulatory period in the sheep. 176 51

The effect of intermittent infusions of somatostatin (SS) on growth hormone (GH) secretion was studied in unrestrained adult male rats deprived largely of SS influence on the medial basal hypothalamus by anterolateral deafferentation (AL-cut). In addition, the influence of hypothalamic surgery on the plasma GH response to beta-endorphin (beta-END) was observed. In sham-operated rats, high-amplitude GH pulses separated by low baseline levels occurred at 185 min intervals. In rats with AL-cut, GH pulses were difficult to identify upon visual appraisal and baseline plasma GH levels became significantly higher than those of sham-operated rats. When AL-cut was performed unilaterally (half-AL-cut), low amplitude GH pulses separated by elevated baseline GH levels occurred at frequent intervals. The amount of GH secreted during 6 h was significantly reduced in rats with AL-cut or half-AL-cut as compared to that of sham-operated rats. The plasma GH response to intracerebroventricular injection of beta-END (4 micrograms) was abolished in AL-cut rats, and the response was significantly reduced in half-AL-cut rats as compared to that of sham-operated rats. When AL-cut rats were subjected to repeated infusions of SS (30 micrograms/kg b. wt./h, 150 min) separated by 30 min control periods, a large rebound of GH secretion was observed after removal and the amount of GH secreted during 6 h became comparable to that of sham-operated rats. The results suggest that SS plays important roles in the dynamic secretion of GH.
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PMID:Effect of intermittent infusions of somatostatin on growth hormone secretion in unrestrained male rats with hypothalamic deafferentation. 196 59

The effect of calcium and magnesium supplementation and the role of opioidergic system was examined in deoxycorticosterone acetate (DOCA)-salt hypertensive rats. The rats were divided into four groups receiving standard laboratory rat diet (control group; n = 9); a calcium-rich diet with 2% CaCl2 added (Ca-group; n = 12); a magnesium-rich diet with 0.5% MgO added (Mg-group; n = 11); and a calcium and magnesium-rich diet with 2% CaCl2 and 0.5% MgO added (Ca/Mg-group; n = 11); each diet contained 7% NaCl. After four weeks on these diets, the rats were decapitated and blood was obtained for the measurement of plasma electrolytes, intraerythrocyte sodium, potassium and magnesium content (RBC-Na, -K, in mEq/L cells and RBC-Mg, in mg/dL cells) and plasma beta-endorphin concentration (beta-END, in pg/mL). In the control group, systolic blood pressure and RBC-Na were obviously higher than in the other groups. Plasma beta-endorphin concentration was 45.1 +/- 13.4 in the control group, 70.7 +/- 17.4 in the Ca-group (P less than .05 v control group), 58.0 +/- 20.1 in the Mg-group and 83.8 +/- 24.8 in the Ca/Mg-group (P less than .01 v control group). The blood pressure correlated significantly with both RBC-Na (r = 0.416, P less than .01) and beta-END (r = 0.436, P less than .005). A negative correlation was also observed between RBC-Na and beta-END (r = 0.437, P less than .005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of Ca and Mg supplementation and the role of the opioidergic system on the development of DOCA-salt hypertension. 200 1

Subcutaneous (sc) administration of 200 micrograms/kg ceruletide (CER), a decapeptide chemically related CCK-8, and 5 mg/kg haloperidol (HLP) to rats increased the plasma immunoreactive beta-endorphin (ir-beta-END) level. The combined injection of CER and haloperidol caused higher plasma ir-beta-END levels than either drug alone. High plasma ir-beta-END levels returned to control levels on the 2nd day. Prior intraperitoneal (ip) administration of a CCK receptor antagonist, L-364,718 (3 mg/kg), but not proglumide (400 mg/kg, ip), inhibited CER-induced, but not HLP-induced, elevation in plasma ir-beta-END levels. The dopamine agonist, bromocriptine (1 mg/kg, ip) decreased plasma ir-beta-END levels, but had not effect on CER-induced elevation in plasma ir-beta-END levels, whereas bromocriptine-induced reduction in plasma ir-beta-END levels was antagonised by HLP. CER injection to chronically HLP-treated rats caused a greater elevation of plasma ir-beta-END levels compared to saline-injected rats. In contrast to the acute experiment, plasma ir-beta-END levels remained elevated over a period of 24 h. In the acute experiment, CER, HLP or the combined treatment with these two drugs had no effect on ir-beta-END contents in the pituitary gland and brain. In the chronic experiment, HLP increased the adenohypophyseal and septal ir-beta-END contents and decreased the hippocampal ir-beta-END contents 24 h after the final HLP injection. CER caused a small reduction only in the hippocampal ir-beta-END contents of CER-injected rats 15 min after injection. When determined on the 2nd day, however, the increases in the adenohypophyseal and septal ir-beta-END contents and the decrease in the hippocampal ir-beta-END contents observed in CER-injected rats were of the same magnitude as those of rats not given the CER injection. These findings indicate that CER stimulates the release of ir-beta-END from the adenohypophysis through CCK-A receptors and that elevated plasma ir-beta-END levels is partly involved in some behavioural effects induced by CER. Furthermore, sustained elevation of plasma ir-beta-END levels after a single injection of CER to chronically HLP-treated rats may explain its long-lasting therapeutic and behavioural effects.
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PMID:Effects of ceruletide and haloperidol on the hypothalamo-pituitary beta-endorphin system and brain beta-endorphin contents in the rat: with special reference to effects of ceruletide in chronically haloperidol-treated rats. 204 84

The neurotransmitter histamine (HA) participates in the neuroendocrine regulation of pituitary hormone secretion and in the regulation of some peripheral hormones. In general, HA has a stimulatory but indirect effect on the release of these hormones by activation of postsynaptic receptors in the hypothalamic region. The release of the pro-opiomelanocortin-derived peptides ACTH, beta-endorphin (beta-END), and alpha-melanocyte-stimulating hormone (alpha-MSH) occurs by stimulation of H1- and H2-receptors and seems to be mediated via release of corticotropin-releasing hormone and vasopressin from the hypothalamus. The HA-induced release of prolactin (PRL) involves H2-receptors in some hypothalamic areas and H1-receptors in other areas. The release of PRL occurs by histaminergic inhibition of tuberoinfundibular dopaminergic neurons and by stimulation of serotoninergic and vasopressinergic neurons. Histaminergic neurons seem to participate in the mediation of the stress-induced release of ACTH, beta-END, alpha-MSH, and PRL. The neurohypophysial hormones vasopressin and oxytocin are stimulated by HA, and a physiological role of HA in the control of vasopressin secretion is likely. HA stimulates the release of peripheral catecholamines and renin. The stress-induced increase in plasma catecholamines and plasma renin activity (PRA) seems also to involve central histaminergic neurons. The effect of HA and stress on peripheral catecholamines is mediated via H1- and H2-receptors, while that on PRA is mediated via H2-receptors.
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PMID:Neuroendocrine functions of histamine. 205 12

Plasma beta-endorphin (beta-END) levels were measured before, after exercise tests and at the onset of spontaneous angina in 23 anginal patients (group 1), 23 patients with silent myocardial ischemia (group 2) and 15 healthy volunteers (group 3). The pain perception in three groups was also measured. Before and after exercise, the concentration of beta-END in group 1 was significantly lower than that in group 2 and group 3. The concentration of beta-END during onset of spontaneous angina was also lower than that of angina-free period in group 1. There was no significant difference of beta-END between group 2 and 3. The values of the pain threshold and tolerance in group 1 were lower than those of group 2 and 3. These data suggested that plasma levels of beta-END may be related to occurrence of angina. The anginal patients had a hypersensitivity and hypotolerance for pain. A positive correlation was found between plasma beta-END and pain threshold, the levels of beta-END might affect the pain perception during the onset of myocardial ischemia.
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PMID:[The role of beta-endorphin and pain perception in silent myocardial ischemia]. 206 Apr 63

The relationship between morphine tolerance and pituitary-adrenocortical activity was examined. In rats made tolerant to morphine by implantation of morphine-containing pellets, there was a significant reduction in plasma levels of beta-endorphin-like immunoreactivity (beta-END-LI), whereas no significant changes in cortisol levels were seen. Naloxone treatment induced an increase in plasma beta-END-LI and cortisol levels in morphine-tolerant animals. Additionally, acute morphine administration induced an increase in plasma levels of beta-END-LI and cortisol, an effect which was prevented by naloxone. These results are consistent with an increased release of pro-opiomelanocortin-derived peptides after acute morphine and with a decreased release of these peptides in tolerant rats, and suggest that opioid peptides play an important role in the regulation of pituitary-adrenocortical function.
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PMID:Plasma beta-endorphin and cortisol levels in morphine-tolerant rats and in naloxone-induced withdrawal. 214 20


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