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)

Ten men and 10 women exercised on a bicycle ergometer for 20 min at 40, 60, and 80% maximal oxygen uptake (VO2max) to determine the relationship between plasma beta-endorphin, catecholamines, and exercise intensity. Compared to rest, plasma beta-endorphins were not significantly elevated during the 40 and 60% workloads (4.8 +/- 1.0 pmol.l-1 vs 3.8 +/- 0.7 and 6.3 +/- 0.9, respectively). In contrast, the 80% exercise significantly elevated endorphins to 16.1 +/- 4.0 pmol.l-1. Plasma norepinephrine concentrations were 0.30 +/- 0.04 ng.ml-1 at rest and increased with exercise intensity (40% = 0.60 +/- 0.05, 60% = 0.93 +/- 0.07, 80% = 2.00 +/- 0.14, VO2max = 2.55 +/- 0.14 ng.ml-1). Plasma epinephrine followed the same trend (rest = 0.07 +/- 0.01, 40% = 0.33 +/- 0.03, 60% = 0.49 +/- 0.02, 80% = 0.88 +/- 0.07, VO2max = 0.95 +/- 0.06 ng.ml-1). Norepinephrine was found to significantly correlate to endorphins (r = 0.499; P less than 0.02). Conversely, epinephrine was not correlated with beta-endorphin (r = 0.309; P greater than 0.05). The low correlation suggests a weak relationship between beta-endorphin and catecholamine responses during exercise. The results of this investigation suggest that the relationship between beta-endorphin and exercise intensity is curvilinear, with anaerobic activity producing the most significant endorphin response. It was also noted that the beta-endorphin response was not related to gender, but the amine response to exercise was gender-related, being greater for the men.
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PMID:Exercise intensity-related responses of beta-endorphin and catecholamines. 296 88

The responses to brief maximal exercise of 10 male subjects have been studied. During 30 s of exercise on a non-motorized treadmill, the mean power output (mean +/- SD) was 424.8 +/- 41.9 W, peak power 653.3 +/- 103.0 W and the distance covered was 167.3 +/- 9.7 m. In response to the exercise blood lactate concentrations increased from 0.60 +/- 0.26 to 13.46 +/- 1.71 mmol.l-1 (p less than 0.001) and blood glucose concentrations from 4.25 +/- 0.45 to 5.59 +/- 0.67 mmol.l-1 (p less than 0.001). The severe nature of the exercise is indicated by the fall in blood pH from 7.38 +/- 0.02 to 7.16 +/- 0.07 (p less than 0.001) and the estimated decrease in plasma volume of 11.5 +/- 3.4% (p less than 0.001). The plasma catecholamine concentrations increased from 2.2 +/- 0.6 to 13.4 +/- 6.4 nmol.l-1 (p less than 0.001) and 0.2 +/- 0.2 to 1.4 +/- 0.6 nmol.l-1 (p less than 0.001) for noradrenaline (NA) and adrenaline (AD) respectively. The plasma concentration of the opioid beta-endorphin increased in response to the exercise from less than 5.0 to 10.2 +/- 3.9 p mol.l-1. The post-exercise AD concentrations correlated with those for lactate as well as with changes in pH and the decrease in plasma volume. Post-exercise beta-endorphin levels correlated with the peak speed attained during the sprint and the subjects peak power to weight ratio. These results suggest that the increases in plasma adrenaline are related to those factors that reflect the stress of the exercise and the contribution of anaerobic metabolism.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The responses of the catecholamines and beta-endorphin to brief maximal exercise in man. 296 9

The subcutaneous administration of beta-endorphin and its endogenic accumulation in the process of elaboration of adaptation to the short-term stress influences is accompanied by the change of chemoreactive properties of rat sensorimotor cortex neurons expressed in increasing of the share of areactive cells and lowering of the share of cells reacting by the response activational form to acetylcholine and noradrenaline led to them microiontophoretically. The reaction intensity of cells, both activational and inhibitory forms to the led neurotransmitters in both experimental groups is significantly lower than in control. The revealed changes of chemoreactive properties of neurons, arising under the influence of the increase of beta-endorphin amount in brain may be one of the mechanisms of its participation in the processes of learning and memory.
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PMID:[Participation of beta-endorphin in the regulation of the membrane chemoreactive properties of the cortical neurons in rats]. 297 1

The neuroendocrine function is regulated by several neurotransmitters (acetylcholine, dopamine, somatostatin and noradrenaline) known to be reduced in brains of patients with Alzheimer's disease (AD). Moreover, the hypothalamus also has pathological changes. In spite of these findings suggesting neuroendocrine dysfunctions, this function has seldom been investigated in AD patients so far. We have compared patients with clinically 'probable' AD of mild-to-moderate severity with nondemented age- and sex-matched controls. Plasma levels of prolactin (PRL), growth hormone (GH) and thyroid-stimulating hormone (TSH) were measured by commercially available radioimmunoassays (RIA) before and after stimulation with metoclopramide, l-dopa or thyrotropin-releasing hormone. Basal plasma levels of beta-endorphin and beta-lipotropin were measured by RIA after high-performances liquid chromatography. Basal and stimulated plasma levels of PRL, GH, TSH and beta-lipotropin were similar in the two groups. Basal lamina levels of beta-endorphin were significantly higher in the patient group. Of doubtful clinical importance, this might be attributed to decreased tuberoinfundibular dopaminergic activity and has also been seen in patients with Parkinson's disease.
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PMID:Neuroendocrinological function in Alzheimer's disease. 297 29

In segments of rabbit ear arteries preincubated with [3H]noradrenaline, Leu-enkephalin, D-Ala2-D-Leu-enkephalin and ethylketocyclazocine concentration dependently reduced the overflow of tritium and the vasoconstriction elicited by field stimulation (120 pulses every 14 min, 1 Hz, 0.3 msec pulse duration). The effects of Leu-enkephalin and ethylketocyclazocine were antagonized by naloxone which, given alone, increased the evoked overflow of tritium at the high concentration of 10 microM. Morphine failed to produce inhibition, and at 100 microM actually increased evoked 3H-overflow. Continued exposure to Leu-enkephalin desensitized the tissue to this opioid; there was no cross-desensitization to ethylketocyclazocine. In arteries not preincubated with [3H]noradrenaline, normorphine, fentanyl and morphiceptin did not change the vasoconstrictor response (5 pulses every min, 5 Hz, 0.3 msec pulse duration). Among various peptide agonists, Leu-enkephalin, D-Ala2-D-Leu-enkephalin and Met-enkephalin were the most potent inhibitors. In a series of peptides with C-terminal extensions of the Met-enkephalin chain, the potency decreased in the order Met-enkephalin greater than Met-enkephalin-Arg-Gly-Leu greater than Met-enkephalin-Arg-Phe greater than BAM-12P greater than beta-endorphin. In a series of peptides with C-terminal extensions of the Leu-enkephalin chain, the potency decreased in the order Leu-enkephalin greater than dynorphin1-13 greater than dynorphin1-9 greater than alpha-neo-endorphin greater than dynorphin1-8 greater than dynorphin1-6 greater than dynorphin1-17. The delta-selective antagonist ICI 154129 counteracted the effect of Met-enkephalin but not that of dynorphin1-13, whereas naloxone counteracted the effect of either agonist.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Presynaptic opioid receptor subtypes in the rabbit ear artery. 298 15

Injection of insulin to fed rats diminished the concentration of fructose 2,6-bisphosphate in white adipose tissue. Incubation of epididymal fat-pads or adipocytes with insulin stimulated lactate release and sugar detritiation and also decreased fructose 2,6-bisphosphate concentration. Such a decrease was, however, not observed in fat-pads from starved or alloxan-diabetic rats. Incubation of adipocytes from fed rats with various concentrations of glucose or fructose led to a dose-dependent rise in fructose 2,6-bisphosphate which correlated with lactate output and detritiation of 3-3H-labelled sugar. In adipocytes from fed rats, palmitate stimulated the detritiation of [3-3H]glucose without affecting lactate production and fructose 2,6-bisphosphate concentration. Incubation of epididymal fat-pads from fed rats in the presence of antimycin stimulated lactate output but decreased fructose 2,6-bisphosphate concentration. Changes in lipolytic rates brought about by noradrenaline, insulin, adenosine and corticotropin in adipocytes from fed rats were not related to changes in fructose 2,6-bisphosphate or to rates of lactate output. In fed rats, the activity of 6-phosphofructo-2-kinase was not changed after treatment of adipocytes with insulin, noradrenaline or adenosine. It is suggested that the decrease in fructose 2,6-bisphosphate concentration observed after insulin treatment can be explained by the increase in sn-glycerol 3-phosphate, an inhibitor of 6-phosphofructo-2-kinase.
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PMID:Regulation of fructose 2,6-bisphosphate concentration in white adipose tissue. 298 73

Body reactions during chain saw work were studied in 14 subjects. The subjects divided into three groups (control, sulpiride, and propranolol) successively cut down logs with a chain saw for seven minutes. The start of the sawing led to a pronounced increase in heart rate which persisted during the sawing. The groups taking sulpiride and propranolol showed a smaller increase in heart rate compared with the controls. Hormonal values (adrenocorticotropic hormone (ACTH), cortisol, adrenaline (Ad), noradrenaline (NA), and dopamine) were increased by the operation. A comparison of these values before and after the operation showed that the increase of cortisol, Ad, and NA values was highest in the controls, intermediate in the propranolol group, and lowest in the sulpiride group. The increase in ACTH, however, was greatest in the sulpiride group, intermediate in the controls and correct in the propranolol group. These findings provide some evidence that chain saw work may have an influence on the whole body, including the hypothalamus and the limbic lobe of the brain.
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PMID:Body reactions during chain saw work. 299 7

Herpes simplex viruses (HSV) remain latent in sensory and peripheral ganglia and can be reactivated to cause recurrent HSV infections. Recent evidence has suggested that stress can induce an immunosuppressive state and increase the frequency and severity of recurrent herpes infections. Because macrophages play a central role in the host defense against HSV, the effects of stress-related neuroendocrine hormones on macrophage-HSV interactions were examined. Norepinephrine and epinephrine blocked the capacity of recombinant interferon-gamma (IFN-gamma) to activate murine macrophages to a cytotoxic state capable of selectively killing HSV-infected cells. In contrast, ACTH, dopamine, serotonin, and beta-endorphin had no effect. The suppression of IFN-gamma-induced, macrophage-mediated lysis of HSV-infected cells occurred concomitantly with a marked increase in macrophage intracellular cyclic AMP levels. Moreover, exogenous administration of dibutyryl cyclic AMP blocked induction of macrophage-mediated cytotoxicity, suggesting that the neurohormones were modulating macrophage function via an adrenergic receptor-mediated system. These findings demonstrate that selective stress-related neurohormones modify the cytolytic activity of macrophages against virus-infected cells and suggest a possible neuroendocrine-immunologic basis for the recurrence of HSV infection.
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PMID:Neuroendocrine hormones suppress macrophage-mediated lysis of herpes simplex virus-infected cells. 300 Nov 83

Hemorrhages of various magnitudes were performed on conscious rats, and arterial pressure, heart rate, and plasma levels of adrenocorticotropin hormone (ACTH), epinephrine, and norepinephrine were measured. Eight rats were prepared with chronic femoral arterial cannulas and received a 10, 15, or 20 ml/kg X 3 min hemorrhage in random order on day 4, 7, or 10 after surgery. Mean arterial blood pressure, heart rate, and plasma ACTH, epinephrine, and norepinephrine concentrations were determined before and 20 min after hemorrhage. Arterial blood pressure decreased significantly immediately after each hemorrhage and slowly recovered over the next 20 min. Heart rate did not change during the 10 ml/kg X 3 min hemorrhage but decreased significantly after 15 and 20 ml/kg X 3 min hemorrhages. Plasma ACTH and epinephrine levels increased significantly 20 min after the 15 and 20 ml/kg X 3 min hemorrhages but not after 10 ml/kg X 3 min hemorrhage. Norepinephrine increased significantly 20 min after the 20 ml/kg X 3 min hemorrhage but not after the 10 or 15 ml/kg X 3 min hemorrhage. There was no significant effect of time and repeated hemorrhages on resting levels of plasma ACTH, epinephrine, norepinephrine, osmolality, or proteins. Since hemorrhage leads to a fall in arterial pressure and a subsequent rise in plasma ACTH, the relationship between plasma ACTH and mean arterial blood pressure during hemorrhage was examined in both conscious and acutely prepared pentobarbital sodium-anesthetized rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Responses of ACTH, epinephrine, norepinephrine, and cardiovascular system to hemorrhage. 301 62

A large body of evidences has suggested the role of adrenergic, opioidergic and other peptidergic receptors in the mediation of animal vas deferens motility. Different animal species showed different neurochemical patterns, so it is to be expected that human vas deferens has its own specific response to several substances, in relation to its peculiar function. In this study we report on the effects of monoaminergic (norepinephrine, dopamine, serotonin, isoproterenol, cholinomimetic drugs) and opioidergic (morphine, buprenorphin, beta-endorphin, met-enkephalin and dynorphin) agonists on isolated human vas deferens motility. Norepinephrine and dopamine provoked complex patterns of motility while opioids did not affect the field electroinduced contractions. The implications of this finding are discussed in relation to human vas deferens function.
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PMID:Receptors mediating contraction of isolated human vas deferens. 302 96


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