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)

Administration of opioid receptor antagonists was utilized to determine the opioid receptor type involved in the suppression of LH release by beta-endorphin (beta-END). Long-term (three to four weeks) ovariectomized rats with chronic third ventricular cannulae were fitted with jugular catheters and received treatment with vehicle or one of three opioid antagonists. The delta antagonist ICI 154, 129, but not the mu1 or mu antagonists naloxazone or beta-funaltrexamine, respectively, blocked the suppressive effect of beta-END on plasma LH levels and transiently but significantly increased LH levels above preinfusion value. None of the antagonists significantly reduced the beta-END-induced release of PRL. These results provide evidence that the inhibitory effect of beta-END on LH release may be mediated by delta receptors.
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PMID:Possible delta receptor mediation of the effect of beta-endorphin on luteinizing hormone (LH) release, but not on prolactin (PRL) release, in the ovariectomized rat. 298 Oct 76

The role of endogenous opioid peptides (EOP) in the neuroendocrine control of primate gonadotropin and PRL secretion was studied in nonrestrained adult male rhesus monkeys. Morphine (0.5-1.0 mg/kg) was used as the prototype opiate, beta-endorphin (beta-END; 10-20 micrograms/kg) and [D-Ala2,D-Leu5] enkephalin (DADLE; 5-20 micrograms/kg) were used as representatives of EOP, and naloxone (0.5-2.0 mg/kg) was used as an opiate receptor blocker. Drugs were administered and blood was collected (at 20-min intervals for 4 h) through an indwelling jugular catheter. LH and PRL levels were measured in plasma by RIA. Intravenous administration of morphine (1.0 mg/kg) and DADLE (10 micrograms/kg) produced decreases in LH levels of 64% and 40%, respectively. These decreases occurred within 1 h after drug injections and lasted for approximately 3 h. beta-END had no effect on LH levels. Naloxone, at all doses studied, significantly increased LH levels (5- to 8-fold). The LH rises occurred within 20 min and lasted for up to 2 h. Both morphine and beta-END produced immediate increases in PRL, which remained elevated for 3 h. DADLE did not alter PRL levels. Naloxone (1.0 and 2.0 mg/kg) decreased PRL concentrations (45% and 60%, respectively). Pretreatment with morphine or DADLE did not alter the LH response to GnRH (100 micrograms) stimulation, indicating a hypothalamic site of action for the opioid inhibition of LH release. Naloxone administration reversed the inhibitory effects of morphine and DADLE on LH. The stimulatory effect of morphine on PRL levels was also reversed by naloxone. These studies further define the postulated physiological role of EOP in primate reproductive neuroendocrinology. Based on receptor selectivities of these opioid agonists, the inhibition of LH may be mediated by delta-receptors, whereas PRL release appears to be mu-mediated.
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PMID:Opioid effects on plasma concentrations of luteinizing hormone and prolactin in the adult male rhesus monkey. 298 Dec 42

This study was designed to compare the amounts of ACTH, beta-endorphin (beta END), and beta-lipotropin (beta LPH) that are present in plasma under basal conditions and after single and repeated administration of a discrete 2-min restraint stress both in intact and in chronically adrenalectomized rats. In intact rats, application of a 2-min restraint stress produced rapid parallel increases in plasma concentrations of radioimmunoassayable ACTH and beta END/beta LPH (the total of beta END-like immunoreactivities), with peaks 2.5-5 min after onset of the stress and return almost to basal concentrations by 30 min. Gel exclusion chromatography [Sephadex G-50 (fine)] and subsequent RIA revealed that plasma obtained from control nonstressed intact rats contained much greater quantities of beta END (94% of the total beta END/beta LPH immunoreactivity) than beta LPH. In contrast, equal amounts of beta END and beta LPH were present in plasma of intact rats 2.5-10 min after onset of the 2-min restraint stress. Chronically adrenalectomized rats lacking glucocorticoid-negative feedback had significantly higher basal plasma concentrations of beta END/beta LPH and ACTH than those present in intact rats. Furthermore, the plasma responses of both beta END/beta LPH and ACTH to stress were markedly enhanced in chronically adrenalectomized rats compared to the corresponding responses in intact rats. Gel exclusion chromatography revealed that both the higher basal concentration and the enhanced plasma beta END/beta LPH response to stress in adrenalectomized rats resulted primarily from increases in the beta LPH component, with lesser increases in the beta END component. In contrast to the proportion in intact rats, in chronically adrenalectomized rats, beta END represented about 27% of the total beta END/beta LPH immunoreactivity in the basal state and about 18% 5-10 min after the onset of restraint stress. In intact rats, the plasma ACTH responses to a subsequent stress applied 5 min (a time when peak plasma levels of hormones are present) or 30 min (a time when the plasma hormone concentrations have returned to prestress levels) after the initial stress and the plasma beta END/beta LPH response to a second stress applied at 30 min were equal to the corresponding hormone responses to a single stress. In contrast, the plasma beta END/beta LPH response to the subsequent stress applied 5 min after the initial stress was significantly potentiated in intact rats.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Differential plasma beta-endorphin, beta-lipotropin, and adrenocorticotropin responses to stress in rats. 298 91

The detailed distribution of adrenocorticotropin (ACTH), beta-endorphin (beta-END) and alpha-melanotropin (alpha-MSH) immunoreactivity was examined in the rat median eminence (ME) and pituitary stalk using light microscopic immunocytochemistry and radioimmunoassay (RIA). Nerve fibers and varicosities immunoreactive for ACTH/beta-END/alpha-MSH had identical distributions in the ME suggesting that they are part of the same arcuate proopiomelanocortin neuronal (POMC) system. The quantitative image analysis of POMC immunoreactive varicosities in the ME indicates no significant differences between the various rostro-caudal segments. In the main (preinfundibular) portion of the ME, a moderate density of immunoreactive elements was located in the lateral part of the internal zone and throughout the postinfundibular ME. Very few scattered varicosities were observed in the neurohemal (external) zone and in the pituitary stalk. By RIA, alpha-MSH is present in a substantially higher concentration than ACTH and beta-END throughout the ME. Knife cuts between the arcuate nucleus and ME indicate that proopiomelanocortin (POMC) fibers enter the ME in its whole rostro-caudal extent. Thus POMC neurons seem to provide innervation of structures in the internal zone but not in the neurohemal/external/zone where the portal capillary system is located. Moreover, the observation that the density of immunoreactive elements is substantially lower in the pituitary stalk than in the ME, suggests that the majority of immunoreactive fibers in the internal zone are not fibers of passage directed towards the neurohypophysis.
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PMID:Topographical distribution of pro-opiomelanocortin-derived peptides (ACTH/beta-END/alpha-MSH) in the rat median eminence. 298 39

By the use of two different double-staining techniques (simultaneous staining of adjacent serial sections and the double-staining elution method) it was possible to demonstrate that a corticotropin-releasing factor (CRF) immunofluorescence co-existed with an adrenocorticotropin (ACTH) and beta-endorphin (beta-END) immunoreactivity, but not with a Met-enkephalin (Met-ENK) immunostaining, within perikarya subpopulations of both the myenteric and submucousal plexus of the rat duodenum. Not a single Met-ENK-positive neuronal cell body was stained also for CRF, ACTH or beta-END. Even nerve fibres, localized in both the myenteric plexus and closely to submucousal blood vessels (probably arterioles), revealed a CRF immunofluorescence, which is also colocalized with an beta-END staining. These results are quite different to the recent observations in the mammalian hypothalamus, suggesting that some myenteric and submucousal plexus neurons may synthesize CRF as well as beta-END and ACTH, but not Met-ENK. The colocalized peptides might be concomitantly released into the synaptic cleft after terminal stimulation.
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PMID:Corticotropin-releasing factor: immunohistochemical colocalization with adrenocorticotropin and beta-endorphin, but not with Met-enkephalin, in subpopulations of duodenal perikarya of rat. 298 78

The effects of agents representing three classes of benzodiazepine receptor-acting drugs on circulating levels of beta-endorphin-like immunoreactivity (beta-END-LI) were examined in male rats. The active benzodiazepine receptor antagonists, ethyl-beta-carboline-3-carboxylate (beta-CCE, 30 mg/kg), methyl-beta-carboline-3-carboxylate (3 mg/kg), and 2-phenylpyrazolo [4,3-c]quinolin-3(5H)-one (CGS-8216, 3 mg/kg), all evoked 3- to 4-fold increases in plasma levels of beta-END-LI as compared to control values. The beta-CCE-induced rise in circulating beta-END-LI was significantly attenuated by pretreatment with the agonist diazepam (2.5 mg/kg) and the antagonist ethyl-8-fluoro-5,6-dihydro-5-methyl-6-oxo-4H-imidazo-[1,5-alpha] [1,4]benzodiazepine-3-carboxylate (Ro 15-1788, 10 mg/kg) but was unaltered by morphine (1 and 5 mg/kg). Ro 15-1788 also significantly attenuated the methyl-beta-carboline-3-carboxylate- and CGS-8216-induced release of pituitary beta-END-LI in vivo. Morphine (5 mg/kg) and diazepam (5 mg/kg) together, but neither alone, significantly reduced the rise in plasma beta-END-LI due to physical immobilization or foot shock. Pretreatment with dexamethasone (100 micrograms), an inhibitor of pituitary anterior lobe (AL) beta-END-LI secretion, completely prevented the plasma beta-END-LI increase due to beta-CCE. Chromatographic analysis of plasma beta-END-LI revealed that most of the beta-END-LI secreted in response to beta-CCE and CGS-8216 resembles beta-lipotropin (beta-LPH), a marker for beta-END-LI release from the AL, in molecular size. Results of in vitro studies indicate that the effects of the anxiogenic agents, beta-CCE and CGS-8216, on AL beta-END-LI release in vivo were not mediated by direct actions of these agents on the pituitary gland. Together, these findings suggest that an interaction exists between a benzodiazepine receptor mechanism(s) and regulation of hypothalamic corticotropin-releasing factor(s) which in turn controls beta-END-LI secretion from the AL of the rat pituitary gland.
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PMID:Evidence that a benzodiazepine receptor mechanism regulates the secretion of pituitary beta-endorphin in rats. 299 Aug 51

Serotonin and dopamine neurons have been shown to exert a stimulatory and inhibitory control, respectively, over pituitary release of beta-endorphin-like immunoreactivity (beta-END-LI). In the present study we sought to determine whether an interaction exists between these two reciprocal mechanisms regulating beta-END-LI in the rat. The intraperitoneal (i.p.) administration of 5 mg/kg quipazine, a serotonin receptor agonist, or 2.5 mg/kg haloperidol, a dopamine receptor antagonist, each elevated circulating levels by beta-END-LI 5-fold over control levels by 30 min post-injection. Pretreatment (1 h) with 5 mg/kg, i.p., cinanserin, a serotonin receptor antagonist, completely blocked the quipazine-induced rise in beta-END-LI without affecting the elevated levels of beta-END-LI in haloperidol-treated animals. Conversely, pretreatment (2 h) with 1 mg/kg, i.p., bromocriptine, a dopamine receptor agonist, had no effect on quipazine-induced release of beta-END-LI but did completely prevent the rise in plasma beta-END-LI due to haloperidol treatment. Gel filtration chromatography revealed that quipazine and haloperidol treatments elevated plasma levels of both beta-END-size immunoreactivity and beta-lipotropin (beta-LPH)-sized immunoreactivity though to different relative degrees. However, since circulating levels of beta-LPH serve as a marker for anterior lobe (AL) beta-END-LI secretion, serotonin and dopamine appear to exert stimulatory and inhibitory control, respectively, over AL beta-END-LI release. Further, the quipazine-induced rise in total plasma beta-END-LI primarily resembled beta-LPH in size and was blocked by cinanserin but not bromocriptine pretreatment. And conversely, bromocriptine but not cinanserin prevented the haloperidol-induced rise in circulating beta-END-LI.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serotonin and dopamine independently regulate pituitary beta-endorphin release in vivo. 300

Open field behavior was observed in conjunction with mating behavior to discern whether the effect of intraventricular (ICV) beta-endorphin (beta-END) on sexual behavior may be secondary to akinesia. Three groups of ovariectomized, estrogen-progesterone-primed rats each received counterbalanced treatments of saline ICV, 2 micrograms beta-END ICV, or 2 micrograms beta-END ICV in combination with a selective opioid receptor antagonist. Receptive behavior (lordosis) and proceptive behaviors (presentation and ear wiggling) were consistently suppressed by beta-END, while ambulation was unaffected. Rearing and grooming were generally decreased, although this effect was statistically significant in only one experiment. Pretreatment with the mu-1 antagonist naloxazone (50 mg/kg intravenously) reversed the effects of beta-END on all behaviors tested. The delta receptor antagonist ICI-154,129 (12.5 and 50 micrograms ICV) only partially reversed the sexual effects of beta-END but completely reversed the open field effects. It is concluded that the suppressive effect of beta-END on sexual behavior, while not behaviorally specific, is not secondary to opioid-induced akinesia.
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PMID:Behavioral specificity of beta-endorphin suppression of sexual behavior: differential receptor antagonism. 301 64

The in vitro and in vivo effects of naloxone (NAL) and endogenous opioids namely methionine and leucine enkephalins (MET-ENK, LEU-ENK) and beta-endorphin (BETA-END) on the brain and lung angiotensin converting enzyme (ACE) activities were investigated. All three peptides dose -dependently inhibited ACE activity in vitro except 10(-5) M concentration of BETA-END which increased the lung ACE activity. NAL which intensified the in vitro inhibitory effect of the used opioids showed an antagonistic effect on the in vivo suppressive effect of BETA-END on both brain and lung ACE activities whereas it had neither antagonistic nor synergistic effect on the in vivo inhibiting effect of MET-ENK and LEU-ENK on the lung ACE activity. The results were consistent with those obtained by using morphine and NAL. As a result the possible contributory action of the excessively released endogenous opioids to overcome shock via their inhibiting effect on ACE was discussed.
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PMID:The in vitro and in vivo effects of enkephalins and beta-endorphin on ACE activity in mice. 301 70

We measured basal plasma concentrations of the immunoreactive (IR) proopiomelanocortin (POMC)-derived peptides ACTH, beta-lipotropin (beta LPH), beta-endorphin (beta END), and alpha MSH in 160 normal dogs, 32 dogs with Addison's disease, 42 dogs with adrenocortical tumors causing Cushing's syndrome, and 169 dogs with pituitary-dependent Cushing's disease. In normal dogs, plasma IR-POMC peptide levels were similar to those in man, except that IR-alpha MSH, a pars intermedia POMC product, was readily detected. In Addisonian dogs, plasma cortisol was decreased, and the IR-POMC peptides were increased, except for IR-alpha MSH, which was normal. In 7 Addisonian dogs given dexamethasone, elevated plasma IR-ACTH, beta LPH, and beta END levels fell dramatically. In dogs with Cushing's syndrome due to adrenal tumors, plasma IR-ACTH, beta LPH, and beta END were decreased, and cortisol was increased, but IR-alpha MSH was normal. Dogs with Cushing's disease due to pars distalis tumors had elevated plasma IR-ACTH, beta LPH, beta END, and cortisol, but normal IR-alpha MSH; their plasma cortisol was suppressed by dexamethasone. There appeared to be 2 types of pars intermedia tumors causing Cushing's disease: 1 dexamethasone nonsuppressible and with disproportionately high plasma IR-alpha MSH levels, the other relatively dexamethasone suppressible and with normal to slightly elevated IR-alpha MSH levels. These 2 pars intermedia tumor types may arise from 2 distinct normal canine pars intermedia cell types. Canine Cushing's disease may provide a useful model for variants of the disorder in man.
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PMID:Plasma immunoreactive proopiomelanocortin peptides and cortisol in normal dogs and dogs with Addison's disease and Cushing's syndrome: basal concentrations. 301 56


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