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 role of skeletal muscle thermogenesis (increases in skeletal muscle tone) in the hyperthermic responses of conscious, unrestrained rats given acute or repeated i.p. or i.c.v. injections of morphine sulfate (MS) or beta-endorphin was investigated. Initial blood gas experiments showed that rats given acute i.p. injections of MS caused PO2 and pH to decrease by 60 min postadministration in a dose-related fashion whereas PCO2 increased; with repeated MS administration the respiratory acidosis seen with acute injections was reduced. Acute i.p. injections of MS (1, 10 or 20 mg/kg) caused catalepsy scores, plasma lactate levels and electromyographic (EMG) amplitude to be elevated in a dose-related fashion along with a rise in rectal temperatures (TRS). Surface (tail) temperatures also rose after the acute MS injections but only after the increase in TR. Significant increases in EMG amplitude after acute injections of MS occurred even before TRS increased and, with subsequent naloxone HCl administration (10 mg/kg i.p.), a rapid and marked fall in EMG amplitude occurred before TRS fell back to saline control levels. Acute i.c.v. injections of 1.1 nmol of either MS or beta-endorphin also caused EMG amplitudes to rise significantly before TRS began to increase. Tail temperatures again increased passively after i.c.v. injection of either drug. Subsequent naloxone injections (10 mg/kg i.p.) to these groups also caused EMG amplitudes to decrease before TRS decreased back to control TRS. Repeated i.p. injections of MS (10 mg/kg i.p. daily for 5 days) caused TRS to be higher than those seen after the initial injection but catalepsy scores, plasma lactates and EMG amplitudes were below those respective levels seen upon acute MS administration. Similar chronic findings occurred in other groups of rats given 1.1 nmol of either MS or beta-endorphin i.c.v., when they had been previously given repeated i.p. injections of MS (5 mg/kg i.p. twice daily for 2 days). The results indicate that acute peripheral or central injections of MS or beta-endorphin to conscious rats cause skeletal muscle to be activated, resulting in nonlocomotor, catatonic behavior. This skeletal muscle activation occurs before the rise in TR and is thought to be an important and possibly the primary cause of the resultant hyperthermia seen in rats after acute central or peripheral administration of MS or beta-endorphin. Repeated injections of morphine cause TRS to escalate higher, compared to that seen with acute MS administration, yet catalepsy scores, plasma lactate levels and EMG amplitude changes did not increase likewise.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Skeletal muscle thermogenesis: its role in the hyperthermia of conscious rats given morphine or beta-endorphin. 295 69

Pregnant rats were injected with saline or L-tyrosine methylester HCl (200 mg/kg) and subjected to an acute forced immobilization stress on day 20 of gestation. At 10, 30, 60, and 120 minutes after the onset of stress, their fetuses were dissected out, and the contents of hypothalamic and pituitary immunoreactive beta-endorphin (IR-beta-EP) and hypothalamic immunoreactive growth hormone-releasing factor (IR-GRF) were determined by specific radioimmunoassays. The maternal stress arose a significant decrease of hypothalamic IR-beta-EP at 30 minutes, while pituitary IR-beta-EP slightly elevated at 30 minutes, then declined at 60 minutes. Hypothalamic IR-GRF showed a gradual increase during the maternal stress. Tyrosine supplementation tended to attenuate stress-induced changes in hypothalamic and pituitary IR-beta-EP, but the response of hypothalamic IR-GRF was less modified by tyrosine. These results showed the functional changes in fetal central beta-EP and GRF under maternal stress in the late gestational life, and suggested that catecholaminergic regulations participate, at least in part, in the fetal neuroendocrine response to maternal stress.
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PMID:The effect of an acute maternal stress on beta-endorphin and growth hormone releasing factor in the rat fetus. 296 92

From neurointermediate lobe (NIL) extracts of two species of Cyprinidae, Carassius auratus and Cyprinus carpio, several peptides were separated by high-performance liquid chromatography (HPLC) on a C18 muBondapak column eluted with a methanol/acetic acid/triethylamine mixture. Monitoring all fractions by radioimmunoassay (RIA) with an antibody against melanocyte-stimulating hormone (MSH) C terminal gave positive reactions for fractions 7, 11-12, 15-16, 23-24, and 25-27. For further characterization, the elution positions of these peaks were compared to those of known synthetic reference substances. Peak 7 elutes in the same position as oxidized alpha MSH, whereas peak 15-16 matches the elution position of des-acetyl alpha MSH and 23-24 that of alpha MSH. The product from peak 26-27 has several characteristics of the diacetylated form of alpha MSH: its immunoreactivity in RIA, its sensitivity to weak bases and to HCl and its mass spectrum which is identical with that of mammalian diacetyl alpha MSH. In both species, the diacetylated form is predominant in the intracellular pool. This study establishes the coexistence of three different forms of alpha MSH, a des-acetylated, monoacetylated, and diacetylated in the cyprinid NIL extracts.
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PMID:Separation and partial characterization by high-performance liquid chromatography and radioimmunoassay of different forms of melanocyte-stimulating hormone from fish (Cyprinidae) neurointermediate lobes. 298 88

The intraperitoneal (i.p.) injection of ACTH 1-24 (0.2 microgram/kg), lysine--vasopressin (10.0 micrograms/kg) or epinephrine HCl (5.0 micrograms/kg) shortly after training or prior to testing caused memory facilitation of a step-down inhibitory avoidance task in rats, acquired with low intensity training footshocks (0.3 mA, 60 Hz). Naloxone HCl (0.4 mg/kg) potentiated their posttraining effect, but antagonized their pre-test effect. Naloxone on its own caused retrograde memory facilitation but had no effect on the test session. Posttraining human beta-endorphin (1.0 microgram/kg) was amnestic, and its pre-test administration enhanced retention. Both effects were naloxone-reversible. Neither the pre-test facilitation caused by beta-endorphin nor those caused by any of the other drugs (which are possible releasers of endogenous beta-endorphin) were observed in animals in which the influence of endogenous opioids was prevented at the posttraining period by the administration of naloxone. These results are compatible with, and considerably strengthen, the previously advanced hypothesis that learning of this task, and possibly others, depends on a state induced by beta-endorphin after training, and that it would normally be dissociated because this peptide is normally not released during test sessions. In addition, the posttraining facilitation caused by ACTH, vasopressin, and epinephrine stands out as an effect separate from, and in fact normally hindered by, posttraining beta-endorphin release.
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PMID:Influence on memory of posttraining or pre-test injections of ACTH, vasopressin, epinephrine, and beta-endorphin, and their interaction with naloxone. 299 40

The potent opiate radioligands [3H]etorphine, [3H]ethylketocyclazocine (EKC), and [3H]naloxone, bound specifically and saturably to a single class of membrane-binding sites in rat neurointermediate lobe (NIL), with Kd values of 3.7, 24, and 51 nM, respectively. In the hypothalamus (Ht), [3H]etorphine bound to specific and saturable sites with a Kd of 2.9 nM. Binding-inhibition studies with [3H]etorphine and unlabeled etorphine-HCl as well as [3H]EKC and unlabeled EKC, revealed high and low affinity binding sites in rat Ht and NIL as well as in the neural lobe of the bovine pituitary gland. [3H]naloxone also bound specifically to two classes of sites in Ht membranes, but to only a single class of low affinity sites in NIL membranes. Specific binding represented 80-90% of total [3H]etorphine binding, about 75% of total [3H]EKC binding, and 45-55% of total [3H]naloxone binding at 22 C in NIL and Ht, respectively. Relative binding potencies derived from Ki values for binding-inhibition studies of [3H]etorphine with opioid peptides and opiates were: NIL, etorphine-HCl greater than dynorphin A greater than naloxone-HCl greater than dynorphin-(1-9) greater than beta-endorphin much greater than alpha-neoendorphin approximately (Leu5)enkephalin approximately DAGO (Tyr-D-Ala-Gly-NMe-Phe-Gly-ol); Ht, etorphine HCl greater than naloxone-HCl greater than beta-endorphin greater than dynorphin A much greater than DAGO greater than morphiceptin much greater than (Leu5)enkephalin. Specific [3H]etorphine binding was also demonstrable after preincubation of NIL membranes with DAGO and (Leu5)enkephalin and after preincubation of Ht membranes with morphiceptin and (Leu5)enkephalin; such binding could be displaced by nonradioactive dynorphin A. In addition, [3H]etorphine binding to bovine neural lobe was displaceable by naloxone-HCl, with an ED50 of 43 nM. Specific ligands for sigma-opiate receptors, such as (+)SKF 10,047 (N-allylnorcyclazocine), phencyclidine (PCP), and (-)cyclazocine, displaced specifically bound [3H]etorphine and [3H]EKC from NIL membranes only at high (micromolar) concentrations. However, specific [3H]PCP sites were of higher affinity in NIL and Ht membranes, with similar Kd values of 102 and 190 nM respectively, and different concentrations (0.15 and 1.32 pmol/mg protein, respectively). These data have revealed several differences in the opiate-binding properties of rat Ht and NIL membranes.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Opiate receptor subtypes in the rat hypothalamus and neurointermediate lobe. 303 71

The synthetic opioid met-enkephalin analog [D-Ala2, MePhe4, Met(0)5ol] enkephalin (DAMME) and the opiate morphine injected intraperitoneally to rats at doses of 0.5-2 and 5-20 mg/kg, respectively, showed a protective effect on gastric damage induced by oral administration of necrotizing agents (0.6 N HCl or 0.2 N NaOH solutions, 1 ml/rat). The protection was prevented by naltrexone (10 mg/kg s.c.), an opioid antagonist with long-lasting activity. Histological sections of mucosal samples from animals pretreated with morphine (10 mg/kg i.p.) and DAMME (1 mg/kg i.p.) showed less alteration of the columnar epithelium, with a normal glandular structure, than untreated rats. A mediation of prostaglandins is suggested, since indomethacin (10 mg/kg s.c.) significantly reduced the protective effects of opioids.
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PMID:Protection by opioids against gastric lesions caused by necrotizing agents. 335 41

A protein of Mr 25-40 kilodaltons in normal human plasma binds human corticotropin-releasing hormone (hCRH), but not ovine CRH. Binding requires both N- and C-terminal hCRH sequences and has a Kd of 2 X 10(-10) M and a binding site concentration of 1.4 pmoles per ml of plasma. Its binding is not affected by heating to 56 degrees C for 1 h, but is abolished by exposure to 6 M guanidine-HCl, 10 mM dithiothreitol. Binding proceeds rapidly at 37 degrees C and is 75% complete within 4 min. Neither rat nor sheep plasma appears to contain a CRH-binding protein. CRH-binding protein may explain the brief biological action of hCRH as compared to ovine CRH in man and why high concentrations of plasma immunoreactive hCRH in women during third-trimester pregnancy do not cause increased ACTH secretion.
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PMID:Specific high-affinity binding protein for human corticotropin-releasing hormone in normal human plasma. 349 46

The effects of morphine HCl and a synthetic met-enkephalin analogue [D-Ala2,MePhe4,Met(O)5ol]enkephalin (FK 33-824) on gastric damage produced by the intraperitoneal administration of indomethacin (10 mg/kg i.p.) have been investigated. Rats intraperitoneally pretreated with morphine HCl (10 mg/kg i.p.) and FK 33-824 (1 mg/kg i.p.) showed a statistically significant reduction both of the number and intensity of lesions induced by indomethacin. This protection was reversed by naloxone HCl (2 mg/kg i.p.). The protective effect was not related to a reduction of gastric secretion since the antisecretory drug cimetidine (25 mg/kg i.p.) and methscopolamine bromide (10 mg/kg i.p.) did not significantly prevent mucosal damage under the same experimental conditions.
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PMID:Effects of morphine and met-enkephalin analogue on gastric lesions induced by indomethacin. 360 43

Repeated preoptic-anterior hypothalamic (POAH) injections of saline and 10 or 25 micrograms/microliters of beta-endorphin or ACTH were given to groups of male Sprague-Dawley rats. One hr after the fifth injection of beta-endorphin or ACTH, each rat received a POAH injection of naloxone HCl (10 micrograms/microliters). Core (Tre-rectal) and surface (Tt-tail) temperatures, metabolic (VO2) and behavioral responses were recorded 30 min before and 60 min after each drug injection. The initial POAH injection of either dose of beta-endorphin produced a hyperthermia. Peak hyperthermia was reduced in the group given 10 micrograms/microliters of beta-endorphin repeatedly. TtS rose after each beta-endorphin injection but temporally lagged Tre increases. Metabolic rate (VO2) was increased with repeated POAH injections of beta-endorphin. Naloxone reduced the elevated Tre seen with beta-endorphin by increasing Tt's further and reducing VO2. POAH administration of ACTH evoked only a slight hyperthermic Tre response, but elevated TtS and VO2S, due to enhanced grooming and explorative behavior. With repeated ACTH injections, TreS did not change from those on the first day as TtS and VO2 remained enhanced. Naloxone reduced VO2 and TtS of the ACTH-treated rats but TreS still were unchanged. Results suggest that the hyperthermia of unrestrained rats given an acute as opposed to repeated POAH beta-endorphin injections is mediated by different effector mechanisms. With the doses used, the slight and unchanging TreS seen with ACTH occurred because this peptide increased heat production due to locomotor activation yet also exaggerated heat loss by vasodilating the peripheral vasculature.
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PMID:Thermoregulatory (core, surface and metabolic) responses of unrestrained rats to repeated POAH injections of beta-endorphin or adrenocorticotropin. 609 74

Thyropin binding to high affinity receptors on human and porcine membranes was studied at pH 7.4, 37 degrees C, in 10 mM Tris-HCl, 150 mM NaCl, 0.1% albumin. By preincubating the membranes in high salt concentration before binding studies, the number of high affinity receptors could be increased 4- to 8-fold. The salt-induced exposure of high affinity TSH receptors was pH- and temperature-dependent and was maximal at pH 5.0, 37 degrees C in the presence of 1 M (NH4)2SO4. Other salts tested, including NaCl, HN4Cl, and Na2SO4, were also able to increase high affinity THS binding. The receptors exposed by salt were indistinguishable from those present on the membranes before such treatment. They had an affinity constant of 0.5 to 1 X 10(10 M-1, and a high TSH specificity with no inhibition of 125I-TSH binding in the presence of a thousandfold excess of gamma-globulin, thyroglobulin, corticotropin, cholera toxin, and gangliosides. Thyrotropin binding to low affinity TSH binding sites (affinity constant 1 to 3 X 10(7) M-1) measured at pH 6.0, 4 degrees C in 10 mM Tris/acetate, 0.1% albumin was unaltered by pre-exposure of membranes to high salt concentrations. These receptors had low TSH specificity and binding was inhibited by gamma-globulin, thyroglobulin, cholera toxin, and gangliosides. The salt-induced selective exposure of high affinity receptors with unaltered number of low affinity sites is further support for the existence of two separate TSH binding sites on thyroid membranes.
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PMID:Salt-induced exposure of high affinity thyrotropin receptors on human and porcine thyroid membranes. 625 Oct 45


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