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)

Basal levels of immunoreactive (ir) beta-endorphin, corticotropin (ACTH), and prolactin (PRL) in plasma of male rats decrease after dexamethasone pretreatment (400 microgram/kg at 24 hr and 200 microgram/kg at 2 hr before). Inescapable electric footshocks increase ir-beta-endorphin, ACTH, and PRL plasma levels and this effect is blocked by dexamethasone pretreatment. Morphine (20 mg/kg) also increases ir-beta-endorphin, ACTH, and PRL levels. Dexamethasone pretreatment blocks the morphine-induced release of ir-beta-endorphin but does not prevent the morphine-induced release of PRL. Naloxone, the opiate antagonist, decreases basal plasma levels of PRL and partially blocks the stress-induced increase of PRL, but it has no effect on the basal or stress-induced release of ir-beta-endorphin. These results are consistent with the proposal that beta-endorphin may interact with an opiate receptor involved in the regulation of PRL secretion.
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PMID:Stress-induced release of prolactin: blockade by dexamethasone and naloxone may indicate beta-endorphin mediation. 624 73

Serum dehydroepiandrosterone sulfate (DHEAS) was measured in 32 infertility patients who were found to be ovulatory, in 37 women with oligomenorrhea, and in 52 hirsute patients under basal conditions. It was also measured in conjunction with adrenocorticotropic hormone (ACTH) stimulation and dexamethasone suppression in 10 of the hirsute women. Serum DHEAS levels were elevated in only 19% of the infertile women with regular ovulation, in 34% of the oligomenorrheic patients, and in 60% of the hirsute women. Of the C-19 steroids (androgens) measured in the 52 hirsute women, ie, total and unbound serum testosterone (T), androstenedione (A), and DHEAS, unbound serum T was most frequently elevated. Eighty-two percent of the hirsute women had either an elevated serum DHEAS level or an increased unbound T level, suggesting 1) that elevations in unbound serum T may be associated with or result from increased serum DHEAS levels and 2) that only a minority of women with so-called idiopathic hirsutism do not have demonstrable androgen excess. Three of 10 hirsute women with elevated serum DHEAS levels had an increased ACTH-induced rise in DHEAS. Dexamethasone given as a single daily dose of 0.5 mg at bedtime resulted in a marked decrease in serum DHEAS in all of the 10 hirsute patients tested within 2 weeks of therapy. Thus, serum DHEAS is a clinically useful indication of adrenal C-19 steroid secretion. When combined with clinical and other hormonal evaluations, its measurement adds an important dimension to the study of gynecologic endocrinology and infertility.
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PMID:Serum levels of DHEAS in gynecologic endocrinopathy and infertility. 626 Nov 97

The effect of the beta-adrenoceptor agonist isoprenaline on the plasma concentrations of beta-endorphin (beta-E) and beta-lipotropin (beta-LPH) was investigated in conscious rats. Isoprenaline (i.m.) elevated plasma beta-endorphin-like immunoreactivity (beta-EI) as measured by radioimmunoassay of unextracted plasma, with peak values 24 min after drug administration. This effect was dose-dependent. The lowest effective dose of isoprenaline was 15 micrograms kg-1; 240 micrograms kg-1 exerted a maximum effect, raising plasma beta-EI about ten-fold above control values. Plasma vasopressin concentrations also increased in response to isoprenaline following a time-course identical to that of plasma beta-EI. (+/-)-Propranolol (1 mg kg-1) but not phentolamine (10 mg kg-1) rendered isoprenaline (240 micrograms kg-1) injections almost ineffective. Because of the cross-reactivity of beta-LPH in the radioimmunoassay used, plasma was extracted by means of a cation exchange resin and subjected to gel chromatography on a Sephadex G-50 column, avoiding artefactual degradation of the peptides. In isoprenaline-treated rats about 50% of the beta-EI behaved similar to human beta-LPH, whereas 45% co-migrated with human beta-E; immunoreactivity corresponding to beta-LPH or beta-E comprised about 70% or 30%, respectively, in the plasma extract of vehicle-treated rats. Dexamethasone pretreatment reduced the isoprenaline-induced increase in plasma beta-EI by 87%, but left the simultaneous elevation of plasma vasopressin concentrations unchanged. These data demonstrate that isoprenaline stimulates beta-LPH and beta-E release in vivo. The possibility of an interrelationship between vasopressin and beta-E release is discussed.
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PMID:The effect of isoprenaline on plasma concentrations of immunoreactive beta-endorphin and beta-lipotropin in the conscious rat. 627 32

The distinctive chromatographic patterns of beta-endorphin-like immunoreactivity (beta END-LI) released from rat pars distalis (PD) or pars intermedia in vitro as well as the selective inhibitory effects of dexamethasone on PD were used to determine which lobe secretes beta END-LI into plasma after clonidine administration in vivo. Gel chromatography (Sephadex G-50) indicates that cultured PD cells released two major immunoreactive species which coelute with beta-lipotropin (beta LPH) or beta END standards. Conversely, virtually all of the beta END-LI secreted by neurointermediate lobe [pars intermedia plus pars nervosa (NIL)] cells in vitro resembled beta END in size, while none was detected which cochromatographed with beta LPH. Incubation of PD cells with clonidine (10(-6) M) evoked a 2-fold increase in beta END-LI release, while the drug had no effect on beta END-LI released from cultured NIL cells. Dexamethasone (10(-7) M) inhibited the clinidine-induced release of beta END-LI from PD cells, whereas it did not influence the stimulated release of beta END-LI from NIL by isoproterenol (10(-6) M). In vivo administration of clonidine (0.5 mg/kg, ip, for 15 min) increased total plasma beta END-LI from 0.75 +/- 0.16 to 1.35 +/- 0.18 ng/ml; 85% of this rise corresponded to beta LPH as determined by gel chromatography. Prior administration of dexamethasone (60 micrograms/kg, ip, for 4 h) completely prevented the clonidine-induced release of beta END-LI in vivo. These results demonstrate that clonidine probably acts selectively on the PD in vivo to release pituitary beta END-LI, and further, that PD can release beta END-LI independently of the pars intermedia.
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PMID:Evidence for independent secretion of beta-endorphin immunoreactivity from rat pars distalis in vivo. 627 37

The purpose of this study was to determine whether or not vasopressin release in response to various stimuli in the conscious rat is controlled by endogenous opioid peptides, in particular beta-endorphin. Naloxone (1 mg.kg-1 i.m.) promoted vasopressin release in response to both an angiotensin II infusion (500 ng . kg-1 . min-1) or an isosmolar, nonhypotensive hypovolaemia achieved by polyethylene glycol injection (PEG, 20% solution i.p.); however, naloxone was without effect when vasopressin release was induced by hypertonic saline injection (2.5% solution i.p.) or a severe fall in arterial blood pressure following trimethidinium (10 mg . kg-1 i.m.) induced ganglionic blockade. Vasopressin release was accompanied by an increase in plasma beta-endorphin-like immunoreactivity (beta-EI) following an angiotensin II infusion of PEG administration, but not after hypertonic saline or trimethidinium injection. Dexamethasone pretreatment (0.5 mg . kg-1 twice i.p.) prevented the increase in plasma beta-EI following an angiotensin II infusion or PEG administration. The simultaneous angiotensin II- or PEG-induced increase in vasopressin release was unaffected or potentiated, respectively, by the glucocorticoid. In contrast, vasopressin release in response to hypertonic saline or trimethidinium injection was significantly inhibited by dexamethasone. We conclude that an inhibitory control by endogenous opiates is involved in some, but not all of the different pathways leading to vasopressin release. The results obtained do not prove but can be reconciled with the proposal that hypophyseal beta-endorphin is the compound responsible.
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PMID:Vasopressin and beta-endorphin release after osmotic and non-osmotic stimuli: effect of naloxone and dexamethasone. 627 72

Immunoreactive ACTH (ir-ACTH) and immunoreactive beta-endorphin (ir-betaEP) were determined in plasma, anterior pituitary, neuro-intermediate lobe, and hypothalamus of sham-adrenalectomized rats, and adrenalectomized rats given six daily injections of vehicle (oil), dexamethasone, 9alpha-fluorocortisol or deoxycorticosterone. 6 d after adrenalectomy, anterior pituitary ir-ACTH and ir-betaEP were double, and plasma levels approximately fivefold those in controls. Adrenalectomy did not alter hypothalamic levels of either peptide, or ir-betaEP in neuro-intermediate lobe, in which tissue ir-ACTH was below detection limit at routine dilutions. Dexamethasone (0.2-200 mug/d) concurrently suppressed plasma ir-ACTH and ir-betaEP, with a near maximal effect at 20 mug, and a half-maximal effect between 2 and 6 mug; similar dose-response characteristics were found for thymolysis. Step-wise increases in anterior pituitary content of both peptides were found, with no change in hypothalamic levels of either peptide, or neuro-intermediate lobe ir-betaEP. 9alpha-fluorocortisol (0.2-200 mug/d) produced plasma, anterior pituitary, and hypothalamic effects equivalent to dexamethasone, but with one-tenth the potency. Unlike dexamethasone, higher doses of 9alpha-fluorocortisol significantly elevated neuro-intermediate lobe ir-betaEP. Deoxycorticosterone (2-2,000 mug/d) produced no significant changes in plasma, anterior pituitary or hypothalamic levels of either peptide; like 9alpha-fluorocortisol, doses of >60 mug/d significantly elevated neuro-intermediate lobe ir-betaEP. Whereas ir-ACTH and ir-betaEP synthesis in and release from the anterior pituitary are under complex negative feedback glucocorticoid control, there exists a mineralocorticoid-specific effect on neuro-intermediate lobe content of ir-betaEP.
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PMID:Glucocorticoid and mineralocorticoid effects on adrenocorticotropin and beta-endorphin in the adrenalectomized rat. 627 99

This study was to ascertain the effect of naloxone and dexamethasone on vasopressin and beta-endorphin release in the rat during inescapable electric foot shock stress. Plasma vasopressin concentrations were not affected by electric foot shock in vehicle-treated rats, but were raised significantly by the stress in animals pretreated with naloxone. The stress-induced increase in plasma beta-endorphin-like immunoreactivity (beta-EI) was similar whether the rats had received naloxone or not. Plasma beta-EI consisted of equal amounts of beta-endorphin-like and beta-lipotropin-like material as revealed by gel filtration. Dexamethasone almost abolished the foot shock-induced increase in plasma beta-EI and, in the presence of dexamethasone, stress was now effective in elevating plasma vasopressin concentrations. These results are consistent with the hypothesis that beta-endorphin, released from the anterior pituitary, inhibits the release of vasopressin from the posterior lobe of the pituitary gland during foot shock-induced stress.
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PMID:Evidence for inhibition by beta-endorphin of vasopressin release during foot shock-induced stress in the rat. 628 77

gamma MSH, a putative hormone in the N-terminal region of the ACTH/beta-endorphin (beta-EP) precursor protein, was studied by RIA with an antiserum against gamma 3MSH in ACTH-producing mouse pituitary tumor cells, AtT-20/D16v. Serial dilution of the culture medium or the cell extract gave parallel lines to the standard curve in the RIA for gamma MSH. Rat median eminence extracts enhanced the release of gamma MSH-like immunoreactivity (gamma MSH-LI) concomitant with ACTH-like immunoreactivity (ACTH-LI) and beta-EP-like immunoreactivity (beta-EP-LI). Dexamethasone suppressed the release of gamma MSH-LI as well as ACTH-LI and beta-EP-LI. Gel exclusion chromatography of the culture medium and the cell extract has revealed that gamma MSH-LI consists of two peaks; one eluted near the elution position of beta-lipotropin and the other near the elution position of beta-EP. There was no peak corresponding to the elution position of synthetic gamma 3MSH. However, sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) has demonstrated that gamma MSH-LI migrated at five positions with molecular weights of 31K, 21-23K, 16-17K, 13-14K, and 3.8K, respectively. The 31K gamma MSH coincided with the migration position of 31K ACTH of 31K beta-EP, and 21-23K gamma MSH coincided with the position of 21-23K ACTH on SDS-PAGE. The 16-17K gamma MSH coincided with the mouse 16K fragment (reported by Eipper and Mains) of ACTH-beta-lipotropin precursor protein in the migration in SDS-PAGE and in immunoreactivity to anti-gamma MSH antiserum. [3H]Glucosamine was incorporated into 16K, 13K, and 3.8K gamma MSH. These results suggest that AtT-20/D16v cells produce gamma MSH-LIs with molecular weights of 31K, 21-23K, 16-17K, 13-14K, and 3.8K, and they are secreted concomitantly with ACTH-LI and beta-EP-LI.
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PMID:Characterization of gamma-melanotropin-like immunoreactivity and its secretion in an adrenocorticotropin-producing mouse pituitary tumor cell line. 628 79

ACTH and lipotropins (beta- and gamma-LPH) are synthesized from a common precursor by the pituitary corticotropic cell. We have measured LPH plasma levels under physiological and pathological conditions and we have compared them with ACTH plasma levels in the same circumstances. Spontaneous variations (nycthemeral rhythm) in LPH, ACTH and cortisol plasma levels were parallel, while responses to Dexamethasone freination test and stress (Insulin induced hypoglycemia) or more specific stimulation (Metopirone, lysine-vasopressin) were parallel and superimposable. LPH levels were always higher than ACTH levels in two pathological circumstances: chronic renal failure and Cushing's syndromes with ectopic ACTH producing tumors. The determination of both ACTH and LPH levels assists the diagnosis of corticotropic insufficiency and etiologic investigation of Cushing's syndrome, after hypercorticolism had been established. Although unable to confirm the presence of corticotropic adenoma in patients with Cushing's disease, or the predict effectiveness of pituitary surgery, these determination bring good arguments for treated Cushing's diseases follow up.
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PMID:[ACTH, beta-endorphin and lipotropins: physiopathological studies in man (author's transl)]. 628 91

Several alterations are present in the hypothalamic hypophyseal regulation of many hormones in patients with chronic renal failure. Evaluation of the hypothalamic hypophyseal adrenal axis in these groups of patients demonstrated normal levels of plasma cortisol. Dexamethasone suppression is abnormal after administration of 1 mg of oral dexamethasone, but normal after 3 mg. Dexamethasone blood levels were lower than the control after administration of 1 mg of oral dexamethasone. A dexamethasone metabolic clearance showed a similar half-life between the patients and controls. Oral absorption study showed poor absorption of the drug. Therefore, there is a problem of gastrointestinal absorption producing the abnormal dexamethasone suppression test in patients with renal failure. Results of metyrapone tests were normal. Corticotropin stimulation tests elicited a normal response. Insulin-induced hypoglycemia does not produce an increment in plasma cortisol or adrenocorticotropic hormone levels.
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PMID:Evaluation of the hypothalamic hypophyseal adrenal axis in patients receiving long-term hemodialysis. 628 45


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