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)

Pentobarbital anesthesia causes about a 10-fold increase in the antinociceptive potency of beta-endorphin microinjected into the periaqueductal gray (PAG) region of the rat brain. The antinociceptive response to PAG morphine was markedly attenuated during anesthesia, but returned as the rats regained consciousness. As they recovered from anesthesia, muscular rigidity and body stiffness (catalepsy) also occurred in the pentobarbital treated animals receiving morphine. These results are consistent with the activation of separate and distinct descending pain inhibitory neuronal systems by these two opioid agonists, and the differential modulation of the systems by pentobarbital. They also suggest that the mechanism underlying muscular responses to morphine is sensitive to pentobarbital, and is not shared by beta-endorphin.
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PMID:Antinociception from the administration of beta-endorphin into the periaqueductal gray of rat is enhanced while that of morphine is inhibited by barbiturate anesthesia. 149 80

The role of beta-endorphin in testicular steroidogenesis is poorly understood. To address this issue, we treated adult hypophysectomized rats intratesticularly with either saline-50% polyvinylpyrrolidone (SAL-PVP) or human beta-endorphin (0.5 microgram/testis; a total of 1 microgram/rat/day) in SAL-PVP for 3 days. Testicular injections were made under ether anesthesia. On Day 3, rats also received injections (s.c.) of either SAL-PVP or 5 micrograms beta-endorphin in SAL-PVP to minimize the dilution of ether in the testis. One hour later, rats were treated (i.p.) with either saline or ovine LH (25 micrograms/rat). One hour after saline or LH injection, blood was obtained via heart puncture for determination of plasma progesterone (P), androstenedione (A-dione), and testosterone (T) levels. The effects of beta-endorphin (50 ng, equivalent to 13.9 pM; or 250 ng, equivalent to 69.6 pM) on P and androgen secretions in vitro were also examined. Intratesticular injections of beta-endorphin significantly (p less than 0.025) decreased the T response to LH treatment, but failed to affect plasma P and A-dione levels. Response of P to LH treatment was increased (p less than 0.005) in medium containing testicular fragments exposed to 250 ng (69.6 pM) beta-endorphin. However, beta-endorphin attenuated LH effects on A-dione and T production in vitro. These studies demonstrate that beta-endorphin inhibits T secretion, possibly because of its effect on the synthesis of T precursors. Thus, testicular beta-endorphin modulates the endocrine function of the testis in adult rats.
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PMID:The influence of beta-endorphin on testicular endocrine function in adult rats. 163 37

We conducted a prospective evaluation of the comparative effects of lumbar epidural and general anesthesia on the hemodynamic and neuroendocrine stress response to cesarean delivery in 21 women with severe preeclampsia. In the epidural group (n = 11), anesthesia extending to the T-4 dermatome level was obtained using 2% plain lidocaine in divided doses. In the general anesthesia group (n = 10), anesthesia was induced after pretreatment with labetalol or nitroglycerin. In the epidural group, mean arterial pressure (MAP) gradually decreased from 133.3 +/- 5.6 mm Hg to 119 +/- 4.4 mm Hg (P less than 0.002). After pretreatment with labetalol or nitroglycerin, MAP in the general group decreased from 131.5 +/- 4.9 mm Hg to 112.2 +/- 3.5 mm Hg (P less than 0.001). At skin incision (after tracheal intubation), MAP increased from 112.2 +/- 3.5 mm Hg to 143 +/- 5.4 mm Hg (P less than 0.001); however, this was not significantly different from baseline MAP. In the epidural group, there were no further changes in MAP. The difference in MAP at skin incision and postpartum period between the two groups was significant (P less than 0.004 and P less than 0.009, respectively). In the general anesthesia group, both adrenocorticotropic hormone and beta-endorphin-like immunoactivity increased significantly from base levels at skin incision. The catecholamines also increased significantly and remained so throughout the study period. In the epidural group, the concentrations of these hormones decreased or remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Anesthetic modification of hemodynamic and neuroendocrine stress responses to cesarean delivery in women with severe preeclampsia. 153 Jul 30

The modifying impact of anaesthesia on the stress reaction related to surgical trauma was investigated on the basis of the neuropeptidergic parameters of 66 patients who had to undergo a gynaecological radical operation. Anaesthesia was either performed as neuroleptanaesthesia or as epidural analgesia by using bupivacaine in combination with general anaesthesia. The plasma concentrations of substance P and beta-endorphin were taken as neuropeptidergic parameters. Both regulatory peptides show numerous corresponding synergisms. An acceleration of these neuropeptide systems is assumed to be present in severe disturbance of homeostasis. Plasma concentrations of substance P and beta-endorphin were examined at 11 measuring points in the perioperative and intraoperative periods. The plasma concentration of substance P significantly declines in the preoperative period while the concentration of beta-endorphin in the plasma remains at a relatively constant level. In the dynamics of beta-endorphin in the plasma significant differences between the two anaesthetic techniques become apparent in the intraoperative period. Those patients given epidural analgesia have a significantly higher maximum concentration at a later date. This difference is attributed to the possible loss of the adrenal medullary function due to partial sympathetic blocking. Single observations in patients pregnant in the last trimester testify to an extraordinary adaptability at the end of pregnancy.
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PMID:[Beta-endorphin and substance P in the perioperative period]. 171 6

beta-Endorphin levels in the whole rat brain were not changed during acute (25 min) or chronic (48 h) exposure of rats to N2O. However, a significant decrease of beta-endorphin was found in the whole brain, brain stem and subcortex during the withdrawal from chronic exposure to N2O. It has been suggested that decrease of beta-endorphin levels during N2O withdrawal could be ascribed to unspecific stress accompanying drug withdrawal. Decrease of central beta-endorphin during N2O withdrawal might have a significant modulatory effect on transmitter balance, neuronal excitability and corresponding withdrawal behaviour. Furthermore, the decrease of beta-endorphin levels in the whole brain during N2O withdrawal might contribute to the postanaesthesia N2O-excitatory syndrome in humans. This might explain the known therapeutic effect of the opioid drug, meperidine on the excitatory N2O withdrawal phenomena during recovery from N2O anaesthesia in man.
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PMID:Decrease of beta-endorphin in the brain of rats following nitrous oxide withdrawal. 180 19

Ninety-five women undergoing induced abortion were randomly premedicated with oral diazepam, 5 or 10 mg, midazolam 15 mg, or intramuscular placebo, 40-60 min before the induction of anesthesia. Prior to premedication and again prior to the procedure, the women completed the questionnaire sheet for the Profile of Mood States (POMS), and plasma samples for immunoreactive beta-endorphin (ir beta-E) and ACTH were taken. The Oblique Tension-Anxiety (T-A) Factor scores derived from POMS correlated with plasma concentrations of ir beta-E and ACTH after premedication. The T-A scores decreased in women premedicated with diazepam, 5 and 10 mg, or midazolam, 15 mg, but not in women treated with placebo. The women premedicated with midazolam, 15 mg, became more fatigued after premedication. The changes in blood pressure after premedication correlated with T-A scores. A positive correlation was found between heart rate and plasma beta-endorphin concentration. The changes in ir beta-E and ACTH did not correlate with the changes in T-A scores. We conclude that POMS T-A scores are useful for assessment of preoperative anxiety and the effect of premedication. The present study did not provide any reliable proof to confirm the hypothesis of a relationship between plasma concentrations of ir beta-E or ACTH and preoperative anxiety. Since many factors modulate endorphin and ACTH secretion prior to operation, the measurement of endogenous opiates may be of limited value in assessment of the effects of preanesthetic medication.
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PMID:The effect of orally administered diazepam and midazolam on plasma beta-endorphin, ACTH and preoperative anxiety. 185 Sep 46

To determine the role of reflex neural mechanisms for hormonal, metabolic, heart rate (HR), and blood pressure (MABP) changes during static exercise, seven health young males performed 10-min periods of two-legged static knee extension both during control and during epidural anesthesia. Comparisons were made at identical absolute (29 Nm) and relative [15% maximal voluntary contraction (MVC)] force. Afferent nerve blockade was verified by hypesthesia below T10-T12 and attenuated postexercise ischemic pressor response. Leg strength was reduced to 67 +/- 5% of control. At same relative force, increases in MABP and HR occurred more rapidly without than with epidural anesthesia (P less than 0.05). This difference was diminished during identical absolute force. Changes in plasma concentrations of catecholamines followed the pattern of HR and MABP responses, with differences between epidural and control experiments being most pronounced early in the work period. Plasma beta-endorphin was elevated only after control exercise. No response at 15% MVC was found for growth hormone, adrenocorticotropic hormone, insulin, glucagon, cortisol, glycerol, free fatty acids, or glucose (P greater than 0.05). In conclusion, during static exercise with large muscle groups and moderate relative force, modest changes in plasma hormones and metabolites take place. Furthermore, afferent nervous feedback from contracting muscles is important in regulation of blood pressure, heart rate, and catecholamine responses during static exercise in humans.
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PMID:Hormonal, metabolic, and cardiovascular responses to static exercise in humans: influence of epidural anesthesia. 187 83

E2078, a new analgesic is a dynorphin derivative. E2078 shows strong affinity to kappa receptors and is not rapidly cleaved by peptidases. This analgesic is also considered to be free of tolerance and dependence. In the present study, to determine the effect of E2078 on pituitary-adrenocortical function the author administered E2078 (0.001, 0.05, 0.1, 1.0, 10.0 mg.kg-1) by intramuscular injection to 38 adult mongrel dogs under enflurane anesthesia (1.0%) and then investigated the changes in the plasma concentrations of ACTH, cortisol, beta-endorphin, PRA, aldosterone and ADH. In the animal groups which received E2078 at dosages of 0.001, 0.05, 0.1, and 1.0 mg.kg-1, no significant differences in the plasma concentrations of each hormone were detected compared with the control group which received physiological saline by intramuscular injection. However, in the dog group which received E2078 at 10.0 mg.kg-1, the plasma concentrations of PRA and aldosterone were significantly elevated.
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PMID:[Effects of E2078, a new dynorphin derivative, on pituitary-adrenocortical functions in dogs]. 197 31

Analgesia and anaesthesia produced by fentanyl, urethane and ether, but not pentobarbital, occurred concomitantly with an increase in the concentration of plasma beta-endorphin like immunoreactivity (BEIR), probably of pituitary origin. This increase was not associated with significant changes in pituitary or brainstem beta-endorphin content. Pretreatment with naloxone caused a reduction in plasma BEIR increase following Hypnorm, ether and urethane; and in the analgesia following Hypnorm and urethane. Pentobarbital, alone or in combination with naloxone, did not increase the concentration of plasma beta-endorphin. These results may indicate participation of endogenous opioids in the mechanism of action of urethane.
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PMID:Effect of anaesthetics on the release of beta-endorphin-immunoreactivity in rat plasma. 200 54

Whether endogenous opioid peptides were involved in the inhibitory action of the hippocampus (HPC) on luteinizing hormone (LH) release was studied examining the effect of naloxone, an opioid antagonist, on the inhibitory action of electrical stimulation of the HPC and also by examining the effect of metenkephalin administration in the HPC, on preovulatory release of LH in proestrous rats. In rats treated with saline at 13:00 h, either sham stimulation or electrical stimulation of the dorsal HPC, which was performed acutely under ether anesthesia, significantly inhibited the afternoon rise in serum LH. In animals treated with naloxone at a dose of 2.0 mg/kg body weight, the afternoon rise in LH appeared smaller than that in the control group. However, statistical analysis showed no significant difference in LH values compared to the control group. Direct administration of met-enkephalin at a dose of 10 micrograms at 13:00 h through a chronically implanted cannula in the HPC did not induce any significant change in the afternoon rise in LH, regardless of whether it induced behavioral seizures or not. The results suggest that opioid peptides in the HPC do not play a significant role in the inhibitory action of HPC on LH release. Opioids existing in areas other than the HPC may play a certain, but small role.
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PMID:The roles of endogenous opioids in the inhibitory action of the hippocampus on preovulatory luteinizing hormone in rats. 208 31


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