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 various bioactive peptides in the control of secretion of hypothalamic somatostatin into the hypophysial portal blood was examined in anesthetized rats. Hypophysial portal blood was withdrawn at a rate of 5.0 microliter/min into a chilled tube through a cannula placed over the stump of the pituitary stalk and segmented every 20 min by air bubbles. Immunoreactive somatostatin (IRS) in the plasma was extracted with acetic acid and acetone and quantified by RIA. Basal levels (mean +/- SE) of plasma IRS in the hypophysial portal blood were 646 +/- 36 and 317 +/- 44 pg/ml in urethane- and pentobarbital-anesthetized rats, respectively. Under urethane anesthesia, injection of synthetic neurotensin into the lateral ventricle at various doses in the range of 0.016--2 microgram/rat caused a significant and dose-related increase of plasma IRS levels in the hypophysial portal blood, and this effect of neurotensin was significantly (P less than 0.05) suppressed by pretreatment with diphenhydramine (1 mg/100 g BW, iv), a histamine receptor blocker. Enhancement of IRS release by neurotensin was also observed in pentobarbital-anesthetized rats. Intraventricular injection of substance P (10 microgram/rat), beta-endorphin (1 and 5 microgram/rat), or [Met5]enkephalin had no effect on the level of somatostatin in the hypophysial portal blood of urethane-anesthetized rats. These results suggest a release of hypothalamic somatostatin into the hypophysial portal blood in response to intraventricular administration of neurotensin, probably by a histaminergic mechanism.
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PMID:Effect of intraventricular injection of neurotensin and other various bioactive peptides on plasma immunoreactive somatostatin levels in rat hypophysial portal blood. 616 24

Intracerebroventricular (ICV) administration of the peptidase inhibitors amastatin, trasylol, bacitracin, or phe-D-ala and systemic administration of phenylmethylsulfonyl fluoride resulted in one or more of the following responses: analgesia, reduced withdrawal severity in opiate tolerant rats, alterations in motor activity and behavior, hypo- and hyperthermia and others; some of these effects were antagonized by naloxone, suggesting participation of opioid and other endogenous peptides. In addition, peptidase inhibitors enhanced analgesic and other responses to opioid peptides given ICV. Peptidase inhibition affords another method of inducing selective pharmacological responses such as pain relief in individuals resistant to other forms of therapy. ICV administration of beta-endorphin in the rat induces general anesthesia that is instantly reversed by systemic naloxone. Extensions of this work include identification of specific neural pathways that mediate anesthesia and characterization of opiate receptor subtype(s) at these sensitive loci. This approach offers the potential for the design of systemically effective opioid peptide anesthetics with little or no secondary effects and rapid reversibility.
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PMID:Newer concepts of analgesia and anesthesia. 619 95

beta-Endorphin was microinjected into rat brain in order to localize central sites associated with some of its pharmacologic effects: namely, analgesia (inhibition of the tail-flick response), catalepsy and changes in body temperature. Microinjections (1 microliter) were made bilaterally under halothane anesthesia and the effects of beta-endorphin were repeatedly assessed at 15- or 30-min intervals for 2 hr. beta-Endorphin produced analgesia and catalepsy when it was injected at low doses (ED50, 1.3 to 2.7 micrograms) into the medial preoptic area, nucleus accumbens, anterior hypothalamus and the periaqueductal gray-4th ventricular spaces. Brain areas of intermediate sensitivities (ED50, 3.7 to 16 micrograms) were the medial thalamus, posterior hypothalamus and areas around the fasciculus retroflexus. The frontal cortex, striatum and lateral areas of the brain were relatively insensitive (ED50 greater than 17 micrograms) to the effects of beta-endorphin on analgesia and catalepsy. beta-Endorphin had complex effects on body temperature. For example, when beta-endorphin was injected into the nucleus accumbens or preoptic area, low doses (1.1--2.1 micrograms) produced hyperthermia; higher doses (8.5 micrograms) produced hypothermia. The brain regions in which low doses of beta-endorphin elicit pharmacologic effects correspond to the anatomic areas in which the endogenous beta-endorphin system is distributed. Similar correspondence to the endogenous enkephalin system was not obtained.
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PMID:beta-Endorphin: central sites of analgesia, catalepsy and body temperature changes in rats. 624 33

beta-endorphin, administered into the cerebral ventricles of rats, provokes a sequence of behavioural and electroencephalographic (EEG) responses similar to those observed with general anaesthetics used clinically. Initial behavioural and EEG excitation, motor incoordination and exaggerated responsiveness to sensory stimuli are followed by a stage of rigid immobility with maintenance of local reflexes (withdrawal, corneal) and EEG arousal in response to stimulation. Finally, there is immobility associated with both EEG and behavioural unresponsiveness to severely noxious stimuli. Such a state of unconsciousness with complete analgesia defines general anaesthesia. This state was completely and rapidly reversed by the specific opiate antagonist, naloxone. The induction of general anaesthesia by a water-soluble neurohormonal peptide acting at specific receptor sites has important implications for traditional theories of anaesthesia.
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PMID:beta-Endorphin induces general anaesthesia by an interaction with opiate receptors. 626 98

To improve understanding of the role of endorphins in septic shock, we examined the effects of anesthesia, splenectomy, live Escherichia coli infusion, and treatment with naloxone, respectively, on plasma beta-endorphin immunoreactivity (beta-EI) and plasma cortisol in dogs. Baseline levels of plasma beta-EI and cortisol were established in awake dogs. Pentobarbital anesthesia alone did not affect plasma beta-EI, but splenectomy was followed by a significant (P less than 0.001) rise in both plasma beta-EI and cortisol. Infusion of saline over a 3-hour period following splenectomy induced no further increase in plasma beta-EI, but infusion of live E. coli in splenectomized dogs caused a further rise in plasma beta-EI (P less than 0.02). Following induction of septic shock in a separate group of splenectomized animals, treatment with naloxone (3 mg/kg bolus and 2 mg/kg/hr infusion) did not alter the rise in plasma beta-EI. These results confirm release of beta-endorphin during septic shock and further implicate the hypothalamic-pituitary-adrenal axis in its pathophysiology. Based on the finding that naloxone did not affect the dynamics of plasma beta-EI, mechanisms are postulated to explain the therapeutic value of this drug in septic shock.
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PMID:Plasma beta-endorphin immunoreactivity in dogs during anesthesia, surgery, Escherichia coli sepsis, and naloxone therapy. 629 64

Chronic dorsal periaqueductal grey matter electrodes were implanted into adult rats under pentobarbitone anaesthesia. Stimulating these electrodes (25-300 microA) produced behavioural analgesia in 23 of 44 rats tested. In rats given the opiate antagonist naloxone attenuation of this analgesia was seen. In 14 rats displaying behavioural analgesia to periaqueductal grey matter stimulation acute electrophysiological experiments were performed under urethane anaesthesia. Microelectrode recordings were made from neurones, excited by noxious heat or pinch applied to the limbs and tail, and located in the reticular formation of the caudal medulla. Stimulation of the periaqueductal grey matter at an intensity sufficient to produce analgesia in the conscious animal produced direct inhibition of the firing of 62% of neurones tested, excited 23%, had no effect on 14% and attenuated the nociceptive responses of 66%. The inhibitions were characteristically long. Local application of naloxone by microiontophoresis attenuated these long inhibitions in 11 out of 16 neurons tested. Immunohistochemical localization of beta-endorphin containing structures in the vicinity of stimulating and recording sites suggested that the naloxone sensitive inhibition of nociceptive neuronal responses in caudal medulla reticular formation may be due to activation of beta-endorphin fibres descending through the periaqueductal area to the caudal medulla.
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PMID:Naloxone reversible inhibition of reticular neurones in the rat caudal medulla produced by electrical stimulation of the periaqueductal grey matter. 630 97

Plasma beta-endorphin (beta-EP) was measured in 48 women. Twenty-three were in labor. In 13 of the 23 patients in labor, beta-EP was determined prior to and after complete onset of epidural anesthesia, and in 10 women, who served as controls, prior to and after injection of saline into the epidural space as part of the loss of resistance technique, but before injection of the local anesthetic. Venous blood also was obtained for plasma beta-EP determinations from 10 healthy non-pregnant women and from 15 patients scheduled for elective repeat cesarean section and who were not in labor. Human beta-EP was determined by radioimmunoassay following silicic acid extraction of plasma samples and separation of the beta-EP fraction by gel chromatography. In the 10 non-pregnant volunteers, plasma beta-EP averaged 11.3 +/- 1.5 fmol/ml (mean +/- SE) as compared with 43.7 +/- 6.5 fmol/ml observed in the 15 women with term pregnancies who were not in labor (P less than 0.005). In the 13 patients in labor who underwent epidural anesthesia, plasma beta-EP concentrations decreased (P less than 0.005) from 54.5 +/- 9.0 to 28.2 +/- 3.5 fmol/ml, whereas there was no significant change in plasma beta-EP levels in the 10 controls who averaged 64 +/- 20.5 and 55.8 +/- 13.6 fmol/ml prior to and following saline injection. These data confirm that plasma beta-EP levels are significantly higher in women with term pregnancies in labor than in non-pregnant women and also demonstrate that epidural anesthesia during labor is accompanied by a significant decrease in maternal plasma beta-EP concentrations.
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PMID:Effects of epidural anesthesia during labor on maternal plasma beta-endorphin levels. 630 38

Catheterization of the portal vein and stereotaxic implantation of electrodes in the lateral hypothalamic area (LHA) were performed in normal rats after thiopental anesthesia. Immunoreactive glucagon (IRG) and insulin (IRI), glucose, catecholamines, and beta-endorphin were monitored in portal and peripheral plasma, before and during electrical stimulation of the LHA. The influences on glucose and hormone concentrations of propranolol, phentolamine, atropine, and naloxone infusions were also investigated in similar rats. A basal portoperipheral concentration gradient was found for IRG, IRI, and catecholamines, but not for beta-endorphin. The LHA stimulation induced a significant rise in portal catecholamine, IRG, and glucose concentrations; IRI remained unchanged; the portoperipheral catecholamine gradient was augmented. These alterations were not observed after bilateral splanchnicectomy. Propranolol infusion abolished the LHA-dependent IRG and glucose rises. Naloxone reduced the IRG rise significantly. Phentolamine and atropine did not modify the LHA-induced reactions. These results suggest that the glucagon release which follows LHA electrical stimulation depends mainly on beta-adrenergic transmission by the splanchnic nerves. Opioid peptide receptors may modulate this effect.
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PMID:Glucagon release after stimulation of the lateral hypothalamic area in rats: predominant beta-adrenergic transmission and involvement of endorphin pathways. 630 29

The mechanism of the prolonged stimulatory effect of corticotropin (ACTH) on adrenocortical synthesis of cortisol was studied in guinea-pig adrenocortical cells harvested from control animals and from guinea-pigs submitted 24 h before the sacrifice to a prolonged ether anesthesia in an attempt to induce a release of endogenous ACTH. As a result of this in vivo exposure to endogenous ACTH, the maximal capacity to produce glucocorticoids (by 1 X 10(5) cells incubated during 2 h) in response to ACTH increased from 579 +/- 111 ng (control group) to 915 +/- 143 ng for cells from treated animals, whereas the apparent affinity of the steroidogenic response to ACTH remained unchanged. This hyper-reactivity of cells from anesthetized animals was also evident in the presence of dibutyryl cyclic AMP. Moreover, there was increased conversion of exogenous pregnenolone into cortisol by cells from previously anesthetized animals. It was therefore concluded that ACTH increases in a lasting way the activity of steroidogenic pathway leading to cortisol synthesis by adrenocortical cells at sites distal to cyclic AMP generation. Besides an obvious increase of formation of pregnenolone in response to ACTH, it seems that this ACTH-induced enhancement in the capacity of the steroidogenic response to ACTH also implies a prolonged stimulatory influence of the peptide on the post-pregnenolone steroidogenic pathway leading to cortisol synthesis.
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PMID:The stimulatory effect of corticotropin on cortisol biosynthetic pathway in guinea-pig adrenocortical cells. 630 45

The concentration of beta-endorphin was determined in the cortex of the large hemispheres, thalamus, striatum and medulla oblongata of rats with varying duration of ethanol anesthesia and after a single injection of ethanol (2.5 g/kg). The content of beta-endorphin was also measured in the brain of rats which preferred and rejected 15% ethanol during long-term (up to 10 months) alcoholization. The data obtained indicate that ethanol produces a specific effect on the endorphinergic system in different brain structures of animals predisposed to voluntary alcoholization. A possible involvement of the neuropeptide in the formation of alcohol tolerance and physical dependence is discussed.
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PMID:[Effect of one-time and chronic administration of ethanol on the concentration of beta-endorphin in the brain of rats with different alcoholic motivation]. 630 22


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