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 release of beta-endorphin and atrial natriuretic factor (ANF) into hypophysial portal plasma was investigated in male and female Wistar rats. The principal aim of the study was to investigate the possible role of beta-endorphin and ANF in the hypothalamic control of LH and prolactin secretion. In male rats, anaesthetized with urethane, the concentrations of beta-endorphin in portal blood collected immediately after hypophysectomy were within the same range as those in peripheral plasma. Furthermore, electrical stimulation of the median eminence did not increase the portal plasma concentrations of beta-endorphin. In female rats, anaesthetized with alphaxalone, the portal plasma concentrations in long-term (6-8 weeks) or acutely hypophysectomized rats were significantly greater than those in peripheral plasma. In acutely hypophysectomized female rats the concentrations and contents of beta-endorphin in portal plasma collected at 10.00-11.30 h of pro-oestrus were significantly (approximately sixfold) greater than at dioestrus or at 20.00-21.00 h of pro-oestrus, but these changes were not consistently seen in all experiments. In female rats in which the pituitary gland was not removed for portal blood collection, portal plasma contents of ANF remained unchanged throughout the day of pro-oestrus, suggesting that it is unlikely that ANF is involved in the spontaneous LH or prolactin surge. The effects of ovarian steroids on the secretion of hypothalamic ANF and beta-endorphin were determined by measuring the portal plasma concentration of ANF and beta-endorphin on the morning of presumptive pro-oestrus in rats ovariectomized 24 h previously and injected with either oil or oestradial benzoate (OB). Portal plasma contents of ANF were significantly lower in OB- compared with oil-treated rats, suggesting that oestradiol inhibits ANF release into rat hypophysial portal plasma. In contrast, there were no significant between-group differences in the content or concentration of beta-endorphin in portal plasma. Thus, the increased beta-endorphin in the portal plasma of some of the intact animals during the morning of pro-oestrus is not due to the preovulatory surge of oestradiol-17 beta. The output of beta-endorphin into portal blood in long-term hypophysectomized rats was lower than in dioestrous or pro-oestrous rats in which the pituitary gland was removed immediately before portal blood collection.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hypothalamic release of atrial natriuretic factor and beta-endorphin into rat hypophysial portal plasma: relationship to oestrous cycle and effects of hypophysectomy. 183 5

The purpose of this study was to compare the control of adrenocorticotropin (ACTH) and corticosterone secretion in homozygous Brattleboro rats with their syngeneic controls, Long-Evans rats, and with rats of the Wistar strain. Plasma concentrations of ACTH and corticosterone were measured by radioimmunoassay in trunk blood, and corticotropin-releasing factor 41 (CRF-41), arginine vasopressin (AVP), and oxytocin were assayed in hypophysial portal vessel blood. Portal plasma was extracted with methanol for CRF-41 determination, and four different antisera and several different high-performance liquid chromatography (HPLC) systems were used to investigate AVP release. The peripheral plasma concentrations of ACTH and corticosterone were significantly higher in Long-Evans and homozygous Brattleboro than in Wistar rats. This difference was due, at least in part, to an approximately twofold greater release of CRF-41 into hypophysial portal blood of the Long-Evans and Brattleboro compared with Wistar rats. There was no significant difference between the strains in the output of oxytocin into portal blood. While no AVP could be detected in the neural lobe of homozygous Brattleboro rats, a small amount of AVP-like immunoreactivity was detected in unextracted hypophysial portal blood from homozygous Brattleboro rats. However, this AVP-like immunoreactivity was clearly distinct from authentic AVP in several HPLC systems, had no antidiuretic activity, and on gel filtration had a relative molecular mass greater than 5 kD. In contrast, the AVP-like immunoreactivity in hypophysial portal blood from Long-Evans rats co-eluted with authentic AVP in all HPLC systems tested.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of adrenocorticotropin control in Brattleboro, Long-Evans, and Wistar rats. Measurement of corticotropin-releasing factor, arginine vasopressin, and oxytocin in hypophysial portal blood. 285 6

We have investigated the role of adrenal steroids and the opiates in regulating arginine vasopressin (AVP) secretion into the pituitary stalk blood of the rat. The portal plasma concentration of AVP in urethane-anesthetized male rats was 532 +/- 68 pg/ml (mean +/- SEM), while the peripheral plasma AVP concentration in intact urethane-anesthetized rats was 20.7 +/- 5.7 pg/ml. Column chromatography on Sephadex G-25 of an extract of a pool of portal plasma revealed that the material being assayed comigrated with synthetic AVP. Bilateral adrenalectomy (ADX) 5 days before the collection of portal blood elevated portal plasma AVP concentrations approximately 6-fold (655 +/- 124 pg/ml in controls vs. 4090 +/- 504 pg/ml in adrenalectomized animals). Dexamethasone administration (15 micrograms/kg X day) for 5 days prevented the ADX-induced increase in portal plasma AVP concentrations without significantly changing portal plasma AVP concentrations in intact rats. Portal plasma concentrations of beta-endorphin were not changed by ADX or dexamethasone treatment. The iv infusion of morphine sulfate (3 mg/kg) dramatically decreased the concentration of AVP in the portal plasma of the rat (501 +/- 101 pg/ml before morphine vs. 185 +/- 50 pg/ml after morphine). The inhibitory effect of morphine was reversed by naltrexone (1.0 mg/kg), whereas naltrexone alone did not alter AVP secretion. Morphine administration also decreased systemic plasma AVP concentrations in urethane-anesthetized rats (27.1 +/- 6.6 pg/ml in controls vs. 3.3 +/- 1.3 pg/ml in morphine-treated rats). Naltrexone treatment reversed this effect. These results suggest that AVP secretion into pituitary stalk blood is under the inhibitory influence of the adrenal steroids, and the increased concentration of AVP found in portal blood may be partially responsible for the elevated levels of ACTH after ADX. Furthermore, morphine-induced activation of the pituitary-adrenal axis is apparently independent of hypothalamic AVP secretion.
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PMID:The concentration of arginine vasopressin in pituitary stalk plasma of the rat after adrenalectomy or morphine. 293 37

Matched hypothalamo-pituitary portal and jugular blood samples were collected over about 6 h from 7 lactating Corriedale ewes penned with their lambs, and a careful record was kept of ewe/lamb behaviour. Hypothalamo-pituitary portal blood concentrations of beta-endorphin were measured by radioimmunoassay and the secretion rates were calculated; these were related to peripheral plasma prolactin and LH concentrations, and the sucking bouts of the lambs. Basal LH concentrations remained less than 1 ng/ml with 0-2 pulses of 1.5-3.5 ng/ml amplitude per 6-h collection period. Prolactin secretion was episodic with individual baselines varying from 24 to 286 ng/ml, and peak concentrations of 50-631 ng/ml. Portal beta-endorphin was secreted in an episodic pattern with individual baseline secretion rates varying from 0.125 to 0.495 ng/min, and peak secretion rates of 0.768 to 3.216 ng/min. A close correlation was seen between sucking bouts and the secretion of portal beta-endorphin and peripheral prolactin; 86% of sucking bouts resulted in a significant release of beta-endorphin, and 46% of sucking bouts resulted in a significant release of prolactin. These results show that hypothalamic beta-endorphin is released in response to the sucking stimulus. This provides support for the hypothesis that, during lactation, beta-endorphin acts within the hypothalamus to reduce GnRH release and hence depress pituitary gonadotrophin secretion.
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PMID:Hypothalamo-pituitary portal blood concentrations of beta-endorphin during suckling in the ewe. 295 92

A pharmacological approach was used to investigate the serotoninergic control of plasma levels on beta-endorphin (beta-EP) and beta-lipotropin (beta-LPH) in humans. Acute administration of L5-OH-triptophan, the physiologic precursor of serotonin (SE), induced a significant rise in plasma beta-EP and beta-LPH levels both when injected iv (20 and 40 mg) (four normal men) and when administered orally (200 and 400 mg) (seven normal men) (P less than 0.01 vs. placebo). The iv route of administration induced a prompt (mean peak values after 150 min) dose-dependent increase in beta-EP and beta-LPH levels. The responses evoked by oral administration (mean peak values after 130 and 240 min) were not dose dependent. Fluoxetine (15 and 30 mg orally) a blocker of SE reuptake, induced a significant dose-related rise in plasma beta-EP and beta-LPH levels in a group of seven normal men (P less than 0.01) (mean peak values after 150 min). Pretreatment with methysergide, a SE receptor antagonist (3 X 2.8 mg orally, five men), did not induce any significant changes in plasma beta-EP and beta-LPH levels, but blocked the increase in the two hormones evoked by L5-OH-triptophan (40 mg iv). Plasma cortisol levels changed similarly to those of beta-EP and beta-LPH in all the experiments, indicating that putative serotoninergic drugs exert a positive role on the various corticotropin-releasing hormone-mediated secretions.
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PMID:Serotoninergic agonists increase plasma levels of beta-endorphin and beta-lipotropin in humans. 609 10

Mechanical compression of the pituitary stalk with the help of a blunt stereotaxic knife results in posterior pituitary denervation (PPD) and sprouting proximal to the injury, leading to formation of an ectopic neurohypophysis in the stalk. This provides an experimental model for those cases in which traumatic damage severs the nerve fibers to the neural lobe but does not obliterate the hypophysial-portal circulation. The effect of PPD on the hypophysial-portal concentration profile of putative ACTH secretagogues as well as basal and stimulated ACTH secretion in vitro were investigated at varying times after PPD. The contents of arginine vasopressin (AVP) and oxytocin (OT) in extracts of the stalk median eminence 1 week after PPD were markedly elevated, whereas corticotropin-releasing hormone (CRH) content was unaffected. Levels of these three neuropeptides in hypophysial-portal blood collected under anesthesia from the proximal stump of the transected stalk (or the ectopic neural lobe) were measured at weekly intervals in groups of rats after sham or PPD surgery. Hypophysial-portal AVP levels showed a monotonic increase with time after PPD from a 1.8-fold elevation at 1 week post-PPD to a maximum concentration 6-fold greater than that in sham groups at 4 weeks post-PPD. Portal plasma OT levels also exhibited extreme elevation. In contrast, portal plasma CRH levels showed an initial 72% decline 1 week post-PPD. We suggest that mechanical damage to the pituitary stalk and the subsequent sprouting redirected secretion of AVP and OT from the neural lobe to the pituitary stalk. This caused sustained elevations of portal plasma concentrations of AVP and OT. The resulting tonic exposure to AVP and/or OT may down-regulate anterior pituitary receptors to these neurohypophyseal peptides and indirectly decrease CRH release into the portal circulation.
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PMID:Marked changes of arginine vasopressin, oxytocin, and corticotropin-releasing hormone in hypophysial portal plasma after pituitary stalk damage in the rat. 772 Jun 31

The effects of acute stress on growth hormone (GH) secretion and the mechanisms involved in its changes have been investigated in sheep. An acute isolation-restraint stress induced a rapid and significant increase in jugular GH levels in 12 out of 14 rams. GH-releasing hormone (GHRH) and somatostatin secretion during the same stress were studied in 5 animals prepared for hypophysial portal blood collection. A 3.5-fold increase in portal GHRH levels was observed concomitantly with a slight elevation in portal somatostatin. Portal corticotropin-releasing hormone (CRH) and jugular cortisol plasma levels increased during the same stress. Our data suggest that an isolation-restraint stress stimulates GH secretion in the sheep and that GHRH may be responsible for GH response.
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PMID:Acute stress stimulates secretion of GHRH and somatostatin into hypophysial portal blood of conscious sheep. 781 15

The acute effect of the non-tricyclic, pro-serotoninergic, antidepressant drug fluoxetine on inflammatory edema was evaluated in the rat. Fluoxetine significantly and dose dependently reduced the swelling induced by the injection of 10% brewer's yeast suspension in the hindpaw. Both adrenalectomy and hypophysectomy prevented the effect of fluoxetine. In contrast pretreatment with the corticotropin-releasing hormone antagonist alpha-helical CRH-(9-41) did not interfere with the anti-inflammatory action of fluoxetine. Moreover, the drug induced a significant increase of corticosterone plasma concentrations in vivo, whereas, in vitro, it did not stimulate beta-endorphin release from anterior pituitary cells. Our data suggest that fluoxetine exerts a potent anti-inflammatory action by inducing pituitary-adrenocortical activation via serotonin.
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PMID:Fluoxetine reduces inflammatory edema in the rat: involvement of the pituitary-adrenal axis. 782 65

The present study investigated the consequences of prenatal exposure to the 5-hydroxytryptamine (serotonin; 5-HT) uptake inhibitor fluoxetine on central 5-HT2A/2C receptors and receptor-mediated function in male and female progeny. Pregnant rats were administered saline or fluoxetine (10 mg/kg s.c.) daily from gestational day 13 through 20. All litters were fostered to non-treated lactating dams. Fluoxetine did not alter weight gain during pregnancy but did significantly decrease progeny weight at birth (-8%) and at postnatal day (PD) 70 (-14%). Progeny were tested at PD28 (males and females) and PD70 (males) by measuring: 1) (+/-)-[125I]4-iodo,2,5-dimethoxyphenylisopropylamine ([125I]DOI)-labeled 5-HT2A/2C receptors; 2) [3H]paroxetine-labeled 5-HT uptake sites; and 3) the stimulation of adrenocorticotropin, corticosterone and renin after a single injection of the 5-HT2A/2C agonist DOI (2 mg/kg s.c.) to provide an index of 5-HT2A/2C receptor function. At PD28, neither 5-HT2A/2C receptor density nor 5-HT2A/2C receptor-mediated endocrine responses were altered by prenatal exposure to fluoxetine. In contrast, at PD70, the maximal density of hypothalamic 5-HT2A/2C receptors was reduced significantly (-35%) in male progeny of fluoxetine-treated dams. Consistent with the reduction of 5-HT2A/2C receptors, the adrenocorticotropin response to DOI was attenuated markedly and selectively (-58%; P < .05) in PD70 progeny following prenatal exposure to fluoxetine. Basal levels of all hormones measured were unaffected by prenatal fluoxetine. Likewise, fluoxetine did not alter the number of hypothalamic 5-HT uptake sites or the binding of [125I]DOI to cortical 5-HT2A/2C receptors.
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PMID:Delayed decreases in brain 5-hydroxytryptamine2A/2C receptor density and function in male rat progeny following prenatal fluoxetine. 818 30

Met-enkephalin is known to circulate in human and animal plasma in low levels. However, the source(s) of plasma met-enkephalin have not been completely elucidated. It has been proposed that the adrenal gland, sympathetic nerves, pancreas and the gut might be implicated. Recently, markedly elevated levels of met-enkephalin have been documented in the presence of liver disease. To investigate potential sources of met-enkephalin in liver disease, rats with acute cholestatic hepatitis 24 h after gavage with alpha naphthylisothiocyanate (ANIT) 100 mg/kg were studied. Plasma met-enkephalin levels were determined by radioimmunoassay in plasma samples from normal, adrenalectomized, or chemically sympathectomized animals. In control rats, ANIT treatment resulted in a striking 8.7-fold increase in systemic venous met-enkephalin levels (inferior vena cava) (P < or = 0.0005) and a significant increase in peptidase-derived met-enkephalin levels (determined after trypsin/carboxypeptidase B digestion of plasma samples) (P < or = 0.05). ANIT-treatment also resulted in a 5.6-fold increase in portal vein met-enkephalin levels (P < or = 0.005). Portal vein met-enkephalin levels were only 1.2-fold higher than IVC levels in ANIT-treated rats (P < or = 0.05). Plasma activities of the two main enkephalin degrading enzymes, aminopeptidase and enkephalinase, were similar in control and ANIT-treated rats. Chemical sympathectomy, prior to ANIT treatment, decreased the elevation in inferior vena caval met-enkephalin levels by 35% (P < or = 0.005). Adrenalectomy did not alter ANIT-induced increases in circulating met-enkephalin levels (pNS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sympathetic nerves, but not the adrenal gland, contribute to elevated plasma levels of met-enkephalin in rats with acute cholestatic hepatitis. 821 May 12


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