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)

Sodium and water intake and excretion of wild rabbits was studied during intracerebroventricular (icv) infusion of corticotropin-releasing factor (CRF). Icv infusion of 200 and 600 pmol/h for 22 h induced changes in the ingestive and general behavior of animals. Increased consumption of 0.5 M NaCl solution was observed during the day of infusion, accompanied by increased sodium excretion, and food intake was decreased. The rabbits maintained the high sodium turnover, together with a high water turnover, for 2-3 days after the icv infusion stopped. Icv infusion of CRF induced strange behaviour in wild rabbits, they appeared to react with fright to normal daily events around them. The strange behaviour started about two hours after the beginning of icv infusion and disappeared immediately after the infusion stopped. On the basis of present and earlier observations, that systemic administration of adrenocorticotropin (ACTH) and adrenal steroid hormones induce increased sodium turnover, it is proposed that changes in the sodium and water metabolism might constitute part of the general stress reaction of the body.
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PMID:Corticotropin-releasing factor enhances sodium and water intake/excretion in rabbits. 202 32

Factors associated with heat-induced increase in blood prolactin (PRL) were investigated. Ten male volunteers (23.7 +/- 2.2 yr) were exposed to exogenous heating (head-out immersion) in 41 degrees C water (control 37 degrees C) for 30 min with and without face fanning and cooling. In seven of the subjects, endogenous heating was produced by a 45-min exercise in a warm environment (41 degrees C; control 10 degrees C) with and without selective face fanning. Venous blood was collected before and after each trial; blood hormones were analyzed by radioimmunologic techniques. Heat loading, whether exogenous or endogenous in origin, induced significant increases in blood PRL, beta-endorphin, and vasoactive intestinal peptide (VIP) levels. Blood thyrotropin (TSH) level decreased significantly during water immersion and more significantly with face cooling. From measurement in peripheral blood, the differential beta-endorphin, VIP, and TSH responses to selective face ventilation during exogenous and endogenous heat exposures suggest that blood PRL released in heat derives from secretory stimuli that are independent of these prolactinotropic factors.
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PMID:Prolactinotrophic effect of endogenous and exogenous heat loads in human male adults. 203 3

Water soluble peptides are normally not transported through the brain capillary wall, i.e. the blood-brain barrier (BBB). Chimeric peptides may be transportable through the BBB and are formed by the covalent coupling of a nontransportable peptide, e.g. beta-endorphin, to a transportable peptide vector, e.g. cationized albumin, using disulfide-based coupling reagents such as N-succinimidyl 3-[2-pyridyldithio(propionate)] (SPDP). The transcytosis of peptide into brain parenchyma, as opposed to vascular sequestration of blood-borne peptide, was quantified using an internal carotid artery perfusion/capillary depletion method. It is shown that [125I]beta-endorphin is not transported through the BBB, but is rapidly cleaved to free [125I] tyrosine via capillary peptidase. Therefore, chimeric peptide was prepared using [125I] [D-Ala2]beta-endorphin (DABE), owing to the resistance of this analogue to peptidase degradation. The [125I] DABE-cationized albumin chimeric peptide is shown to enter brain parenchyma at a rate comparable to that reported previously for unconjugated cationized albumin. When the [125I] DABE-cationized albumin chimeric peptide was incubated with rat brain homogenate at 37 C, the free [125I] DABE was liberated from the cationized albumin conjugate prior to its subsequent degradation into free [125I] tyrosine. Approximately 50% of the chimeric peptide was cleaved within 60 sec of incubation at 37 C. These studies demonstrate that 1) [125I]beta-endorphin is not transported through the BBB in its unconjugated form, 2) a [125I] DABE-cationized albumin chimeric peptide is transported through the BBB into brain parenchyma at a rate comparable to the unconjugated cationized albumin, and 3) brain contains the necessary disulfide reductases for rapid cleavage of the chimeric peptide into free beta-endorphin and this cleavage occurs before degradation of the [125I] DABE into [125I] tyrosine.
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PMID:Beta-endorphin chimeric peptides: transport through the blood-brain barrier in vivo and cleavage of disulfide linkage by brain. 213 82

Atrial natriuretic peptide (ANP) has been identified in the central nervous system and its participation in regulation of various regulatory brain functions has been postulated. To elucidate whether central ANP influences endocrine systems related to blood pressure regulation and renal excretory functions, effects of infusion of ANP at a rate of 120 ng.min-1 into the third cerebral ventricle on plasma level of epinephrine (E), norepinephrine (NE), renin, vasopressin and beta-endorphin as well as on excretion of urine, sodium, potassium (UKV) solutes and free water (CH2O) were investigated in conscious dogs. Significant decrease of plasma E from 77.6 +/- 7.0 to 62.1 +/- 4.8 pg.ml-1 and of NE from 345.5 +/- 20.7 to 286.4 +/- 15.0 pg.ml-1 was found at the end of 30 min lasting ANP infusion. Significant elevation of PRA and UKV and a decrease in CH2O were found 60 min after ANP infusion. No significant changes in other variables were found. In time control experiments plasma hormones concentration and renal excretory functions were not significantly influenced. The results suggest that central ANP may affect the sympatho-adrenal outflow.
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PMID:Central effects of atrial natriuretic peptide on plasma catecholamines, vasopressin, renin and beta-endorphin and on renal excretory functions in the dog. 214 67

To determine the effect of pregnancy on the plasma beta-endorphin response to exercise in the water, 12 women were tested during the 15th, 25th, and 35th wk of pregnancy and 10 wk post partum. Each trial consisted of 20 min of lateral supine rest on land, 20 min of immersion to the level of the xiphoid in 30 degrees C water, 20 min of exercise at 60% predicted maximal capacity, and 20 min of lateral supine recovery. Resting beta-endorphin concentrations were elevated during the 15th wk (137.4 +/- 77.4 pg.ml-1) compared to post partum levels (19.8 +/- 17.6). However, neither was different from the 25th (65.6 +/- 68.4) or 35th (48.0 +/- 54.4) wk. Immersion increased beta-endorphin during the post partum trials but resulted in no consistent change during pregnancy. Conversely, exercise had no effect on beta-endorphin post partum but significantly elevated it during pregnancy, the greatest increase occurring during the 15th wk compared to the 25th or 35th wk. Twenty minutes after exercise, beta-endorphin returned to resting levels during all trials. It was concluded that the effect of pregnancy on plasma beta-endorphin is greater than the effect of exercise. Furthermore, pregnancy seems to accentuate the exercise-induced increase in beta-endorphin.
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PMID:The beta-endorphin responses of pregnant women during aerobic exercise in the water. 214 48

This study examined antinociception induced through the activation of local opioid receptors in inflammation by endogenous opioids. Rats developed a unilateral localized inflammation upon injection of Freund's adjuvant into one hindpaw. Four to 6 d later they were subjected to cold water swim (CWS), an environmental stimulus known to activate intrinsic opioid systems. Following CWS (1 min) the animals' withdrawal threshold to noxious pressure applied onto the paws increased significantly more on the inflamed paw than on the noninflamed paw. This unilateral antinociceptive effect in inflamed paws was dose-dependently and stereospecifically reversible by intraplantar (i.pl.) but not systemic (i.v. or s.c.) administration of the opioid antagonist naloxone (18 micrograms). This suggested that CWS-induced antinociception in inflamed tissue was brought about by the activation of local opioid receptors. Antiinflammatory or vasoconstrictive events, as measured by paw volume and temperature, did not contribute to this unilateral antinociception. Receptor-selective antagonists indicated the involvement of mu- and delta- but not kappa-receptors. Intravenous application of a universal antibody to endogenous opioid peptides (3-E7) and a specific antibody to beta-endorphin, but not antisera against metenkephalin or dynorphin, abolished the CWS effect. Finally, the i.pl. injection of synthetic beta-endorphin (1-31) produced an antinociceptive effect in inflamed paws which was reversible by i.pl. naloxone and selective mu- and delta-receptor antagonists. These findings suggest that antinociception in inflamed tissue can be induced through the activation of local opioid receptors by endogenous beta-endorphin released during CWS.
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PMID:Intrinsic mechanisms of antinociception in inflammation: local opioid receptors and beta-endorphin. 215 30

It has been shown, that piracetam by i.p. injection (10, 100, 400 mg/kg) or by consumption with drinking water 10, 100, 1000 mg/kg/day during 12 days delays extinction of conditioned reflex of passive avoidance and dose-dependence elevates exploratory activity in "open field", pain sensitivity threshold reduces to 70-75%. Prolonged consumption of 1000 mg/kg/day piracetam results in 3-fold decrease of beta-endorphin concentration in plasma (p less than 0.01) and 100 mg/kg/day--in 35% increase of cAMP content in rat brain cortex.
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PMID:[Effects of piracetam on pain sensitivity and levels of beta-endorphin in blood and cAMP in the cerebral cortex of rats]. 215 15

A 100 plaque forming unit (pfu) dose of a temperature-sensitive (ts) mutant of vesicular stomatitis virus (VSV), tsG31 KS5, engendered a slowly progressive paralytic central nervous system (CNS) disease that killed all BALB/c nude mice within 28 days. Reconstitution of nude mice with 10(7) syngeneic splenocytes 24 h before intracerebral inoculation with tsG31 KS5 VSV, however, protected 92% of the animals from death. When these reconstituted animals were injected intracerebroventricularly with 14 pmol of beta-endorphin 24 h after reconstitution with splenocytes and 24 h before inoculation with tsG31 KS5 VSV, only 72% of the animals survived. Furthermore, whereas 40% of the afflicted reconstituted nude mice given intracerebroventricular injections of sterile water were able to recover from the symptoms of disease, those surviving animals which received beta-endorphin were unable to do so. A single intravenous injection of 14 pmol beta-endorphin, or repeated postinfection administration of 28 pmol of beta-endorphin intravenously into nude mice reconstituted with syngeneic splenocytes, which were pretreated with beta-endorphin, did not alter the course of CNS disease induced by tsG31 KS5 VSV. The effect induced by intracerebroventricular injection of beta-endorphin was antagonized by naloxone, but not by the neuropeptide fragment beta-endorphin-(1-27). A simultaneous intracerebroventricular injection of reconstituted nude mice with 1220 pmol of naloxone and 14 pmol of beta-endorphin resulted in a 89% survival rate, and 33% of the afflicted animals were able to overcome the symptoms of the disease induced by tsG31 KS5 VSV. Intracerebroventricular injection of reconstituted nude mice with 330 pmol of beta-endorphin-(1-27) and 14 pmol of beta-endorphin resulted in a 72% survival rate and the surviving animals were unable to improve appreciably the clinical status of their disease. Injection of reconstituted nude mice with either 1220 pmol of naloxone or 330 pmol of beta-endorphin-(1-27) alone did not alter the course of the CNS disease in any way. A single intracerebroventricular injection of 29 pmol of another psychoactive peptide, [Des-Tyr]-endorphin, 24 h after reconstitution of nude mice with splenocytes and 24 h prior to infection with virus, resulted in 74% survival; and 39% of the afflicted animals were able to recover from the clinical symptoms.
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PMID:Beta-endorphin alters the course of central nervous system disease induced by a temperature-sensitive vesicular stomatitis virus in reconstituted nude mice. 216 Apr 76

This study demonstrates that a chronic osmotic stimulus can influence the hypothalamo-pituitary axis by inhibiting the secretion of basal and adrenalectomy-elevated adrenocorticotropin (ACTH) from the anterior pituitary. In rats given 340 mM NaCl instead of tap water to drink for 12 days, plasma concentrations of ACTH decreased to 105 +/- 27 pM (mean +/- S.E.M., n = 6) compared with control animals (182 +/- 13 pM). In adrenalectomised (ADX) rats given 150 mM NaCl to drink for 12 days, plasma ACTH concentrations were greatly increased (783 +/- 141 pM) but in ADX rats treated with 340 mM NaCl for the same period, plasma ACTH was similar to controls (237 +/- 59 pM). The corticotropin-releasing factor (CRF-41) content of the median eminence (ME) was reduced in ADX rats on 150 mM NaCl (854 +/- 78 fmol) and further reduced in ADX rats given 340 mM NaCl (510 +/- 56 fmol) compared with control animals (1239 +/- 114 fmol), suggesting that the decrease in plasma ACTH concentrations in saline-treated animals is secondary to a decrease in the secretion of CRF-41 from the ME. These data are the first evidence for a central mechanism, independent of glucocorticoid feedback, through which a chronic osmotic stimulus can inhibit the activity of CRF-41 neurons.
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PMID:Inhibition of rat corticotropin-releasing factor and adrenocorticotropin secretion by an osmotic stimulus. 216 61

Snake (Ptyas mucosa) brains (400 g) were extracted with a mixture of acetone, water, and hydrochloric acid. The precipitate (5.6 g) that formed upon addition of five volumes of acetone to the extract, designated acid-acetone powder, was subjected to gel filtration on Sephadex G-25. A large unretarded peak (SB-1) with molecular weight greater than 5000 and a small retarded peak (SB-2) with molecular weight smaller than 5000 were obtained. They were then separately subjected to ion-exchange chromatography on CM-cellulose. Adrenocorticotropic activity was detected in the fractions by their ability to stimulate isolated rat adrenal cells to produce corticosterone. Opiate activity was detected in the fractions by their ability to inhibit the binding of (D-Ala2,D-Leu5)-[tyrosyl-3,5-3H]enkephalin to rat brain membranes and their cross-reactivity in a beta-endorphin radioimmunoassay. Adrenocorticotropic and opiate activities were found to be concentrated in fractions strongly adsorbed on CM-cellulose, which were eluted by combined pH and ammonium acetate concentration gradients. There appeared to be a separation between adrenocorticotropic and opiate activities, suggesting that they were due to separate molecular entities.
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PMID:Adrenocorticotropin- and beta-endorphin-like substances in brains of the freshwater snake Ptyas mucosa. 217 78


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