Influence of endogenous opioids on the response of selected hormones to exercise in humans

1986 ◽  
Vol 61 (3) ◽  
pp. 1051-1057 ◽  
Author(s):  
P. A. Farrell ◽  
A. B. Gustafson ◽  
T. L. Garthwaite ◽  
R. K. Kalkhoff ◽  
A. W. Cowley ◽  
...  
Keyword(s):  
Venous Blood ◽  
Endogenous Opioids ◽  
Psychological State ◽  
Opioid Antagonist ◽  
Plasma Norepinephrine ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Naltrexone Treatment ◽  
The Difference ◽  
Exercise Induced

To examine the influence of endogenous opioids on the hormonal response to isotonic exercise, eight males were studied 2 h after oral administration of placebo or 50 mg naltrexone, a long-lasting opioid antagonist. Venous blood samples were obtained before, during, and after 30 min of bicycle exercise at 70% VO2max. Naltrexone had no effect on resting cardiovascular, endocrine, or serum variables. During exercise epinephrine was higher [mean 433 +/- 100 (SE) pg/ml] at 30 min with naltrexone than during placebo (207 +/- 26 pg/ml, P less than 0.05). Plasma norepinephrine showed the same trend but the difference (2,012 +/- 340 pg/ml with naltrexone and 1,562 +/- 241 pg/ml with placebo) was not significant. Plasma glucose was higher at all times with naltrexone. However, the difference was significant only 10 min into recovery from exercise (104.7 +/- 4.7 vs. 94.5 +/- 2.8 mg/dl). Plasma growth hormone and cortisol increased during recovery and these elevations were significantly (P less than 0.05) augmented by naltrexone. Plasma vasopressin and prolactin increased with exercise as did heart rate, blood pressure, lactic acid, and several serum components; these increases were not affected by naltrexone. Psychological tension or anxiety was lower after exercise compared with before and this improved psychological state was not influenced by the naltrexone treatment. These data suggest that exercise-induced activation of the endogenous opioid system may serve to regulate the secretion of several important hormones (i.e., epinephrine) during and after exercise.

scholarly journals  The role of beta-endorphin in horses: a review

2011 ◽  
Vol 56 (No. 9) ◽  
pp. 423-429 ◽  
Author(s):  
M. Golynski ◽  
W. Krumrych ◽  
K. Lutnicki
Keyword(s):  
Pain Threshold ◽  
Social Activity ◽  
Prognostic Indicator ◽  
Endogenous Opioids ◽  
Oxygen Species ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Beta Endorphin ◽  
Opium Alkaloids

  Opium alkaloids counterparts are secreted by human and animal organisms but the role of endogenous opioid peptides in horses has not yet been fully elucidated. Endogenous opioids are involved in regulating food intake, sexual and social activity, pain relief and pain threshold regulation in horses as well as in regulating the functions of the immune system. The aim of this review is to describe the endogenous opioid system in the horse and its function during stress, illness, reproduction, and its influence on immunity and on the formation of reactive oxygen species (ROS) in horses. What is currently known concerning beta-endorphin suggests that they can be a promising diagnostic or prognostic indicator of many pathologic states in horses.

scholarly journals Adrenocorticotropin Responses to Naloxone in Sons of Alcohol-Dependent Men1

1999 ◽  
Vol 84 (1) ◽  
pp. 64-68
Author(s):  
Gary S. Wand ◽  
Deborah Mangold ◽  
Mahmood Ali
Keyword(s):  
Family History ◽  
Alcohol Dependence ◽  
Study Groups ◽  
Corticotropin Releasing Factor ◽  
Opioid Antagonist ◽  
Endogenous Opioid System ◽  
Plasma Acth ◽  
Endogenous Opioid ◽  
Double Blind ◽  
Alcohol Dependent

The endogenous opioid system is part of a neural circuitry functionally related to alcohol-seeking behaviors. A family history of alcoholism is the strongest predictor of future development of alcohol dependence. This study was designed to evaluate ACTH responses to opioid receptor blockade as a function of family history for alcohol dependence. The nonselective opioid antagonist naloxone stimulates ACTH secretion by blocking opioidergic input on paraventricular corticotropin-releasing factor neurons, thereby providing a methodology for comparing hypothalamic opioid tone between study groups. Sixty nonalcoholic subjects, aged 18–25 yr, were enrolled in a protocol to measure the ACTH response to naloxone. Thirty-two subjects were offspring from families with a high density of alcohol dependence and were designated as family history-positive subjects. Twenty-eight subjects were offspring of nonalcohol-dependent parents and were designated family history-negative subjects. Subjects received naloxone (125 μg/kg) or placebo (0.9% saline) in double blind, randomized order. Plasma ACTH was monitored. Family history-positive men had increased ACTH response to naloxone compared to 1) family history-positive women, 2) family history-negative men, and 3) family history-negative women. Despite differences in plasma ACTH levels after naloxone administration, plasma naloxone concentrations did not differ between study groups. This finding suggests that nonalcoholic male offspring of alcohol-dependent men have altered endogenous opioid activity directed at hypothalamic corticotropin-releasing factor neurons.

Opioids in Remote Ischemic Preconditioning-Induced Cardioprotection

2016 ◽  
Vol 22 (2) ◽  
pp. 112-121 ◽  
Author(s):  
Puneet Kaur Randhawa ◽  
Amteshwar Singh Jaggi
Keyword(s):  
Ischemic Preconditioning ◽  
Ischemia Reperfusion ◽  
Artery Bypass ◽  
Bypass Graft ◽  
Endogenous Opioids ◽  
Remote Ischemic Preconditioning ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Cardioprotective Effects

Remote ischemic preconditioning (RIPC) is an intriguing process whereby transient regional ischemia and reperfusion episodes to remote tissues including skeletal, renal, mesenteric provide protection to the heart against sustained ischemia–reperfusion-induced injury. Clinically, this technique has been used in patients undergoing various surgical interventions including coronary artery bypass graft surgery, abdominal aortic aneurysm repair, percutaneous coronary intervention, and heart valve surgery. The endogenous opioid system is extensively expressed in the brain to modulate pain sensation. Besides the role of opioids in relieving pain, numerous researchers have found their critical involvement in evoking cardioprotective effects. Endogenous opioids including endorphins, enkephalins, and dynorphins are released during RIPC and are critically involved in mediating RIPC-induced cardioprotective effects. It has been suggested that during RIPC, the endogenous opioids may be released into the systemic circulation and may travel via bloodstream that act on the myocardial opioid receptors to induce cardioprotection. The present review describes the potential role of opioids in mediating RIPC-induced cardioprotection.

scholarly journals The aetiology of social deficits within mental health disorders: The role of the immune system and endogenous opioids

2019 ◽  
Author(s):  
Sarah Jane Charles ◽  
Miguel Farias ◽  
R. I. M. Dunbar
Keyword(s):  
Mental Health ◽  
Immune System ◽  
Mental Health Disorders ◽  
Social Bonding ◽  
Endogenous Opioids ◽  
Future Research ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Health Disorders

The American National Institute for Mental Health (NIMH) has put out a set of research goals that include a long-term plan to identify more reliable endogenous explanations for a wide variety of mental health disorders (Insel, 2013). In response to this, we have identified a major symptom that underlies multiple mental health disorders – social bonding dysfunction. We suggest that endogenous opioid abnormalities can lead to altered social bonding, which is a symptom of various mental health disorders, including depression, schizophrenia and ASD. This article first outlines how endogenous opioids play a role in social bonding. Then we show their association with the body’s inflammation immune function, and review recent literature linking inflammation to mental health ‘immunophenotypes’. We finish by explaining how these immunophenotypes may be caused by alterations in the endogenous opioid system. This is the first overview of the role of inflammation across multiple disorders where we provide a biochemical explanation for why immunophenotypes might exist across diagnoses. We propose a novel mechanism of how the immune system may be causing ‘sickness-type’ behaviours (fatigue, appetite change, social withdrawal and inhibited motivation) in those who have these immunophenotypes. We hope that this novel aetiology can be used as a basis for future research in mental health.

Characteristics, Mechanisms, and Health Implications of Exercise-Induced Hypoalgesia

2019 ◽  
Author(s):  
Laura D. Ellingson ◽  
Christopher D. Black
Keyword(s):  
Chronic Pain ◽  
Isometric Exercise ◽  
Exercise Adherence ◽  
Exercise Bout ◽  
Pain Modulation ◽  
Dynamic Resistance ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Exercise Induced ◽  
Sensitivity To Pain

Exercise is known to exert an influence on pain. Specifically, sensitivity to pain decreases both during and following a single bout of exercise—a phenomenon that has been termed exercise-induced hypoalgesia (EIH). EIH has been shown to occur following a variety of types of exercise including aerobic, dynamic resistance, as well as intermittent and continuous isometric exercise, and with a variety of types of pain stimuli including pressure, thermal, and electrical, among others. Depending upon the type of exercise, the intensity and duration of the exercise bout may affect the magnitude of EIH observed. EIH also may be influenced by presence of chronic pain. In individuals with chronic pain conditions, exercise can have both hypo- and hyperalgesic effects, again depending on the specifics of the exercise stimulus itself. The mechanisms underlying EIH have not been definitively established. However, a number of potentially viable mechanisms have been examined including: release of stress mediators such as adrenocorticotrophic hormone and growth hormone (GH), stimulation of the endogenous opioid system, interactions between the pain modulatory system and the cardiovascular system resulting from shared neurological pathways, activation of the endocannabinoid (eCB) system, and engagement of supraspinal pain inhibitory mechanisms via conditioned pain modulation (CPM). There is also some evidence that psychosocial factors, including pain-related beliefs like catastrophizing and expectation, may influence EIH. Research in EIH has several important implications for research and practice. In healthy adults, reduced sensitivity to pain is a salient benefit of exercise and EIH responses may play a role in exercise adherence. For chronic pain patients, research on EIH has the potential to uncover mechanisms related to maintenance of chronic pain. Improving our understanding of how and why hyperalgesia occurs following exercise in these patients can aid in understanding central nervous system mechanisms of disease maintenance and ultimately may help to avoid symptom exacerbation with exercise. However, there remain practical and mechanistic questions to be examined. Translating reductions in pain sensitivity that occur with exercise under controlled laboratory conditions to situations that are more naturalistic will be an important next step for promoting physical activity as a treatment for pain.

Effects of naloxone on the sensation of dyspnea during acute respiratory stress in normal adults

1993 ◽  
Vol 74 (2) ◽  
pp. 590-595 ◽  
Author(s):  
Y. Akiyama ◽  
M. Nishimura ◽  
S. Kobayashi ◽  
A. Yoshioka ◽  
M. Yamamoto ◽  
...  
Keyword(s):  
Minute Ventilation ◽  
Endogenous Opioids ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Specific Effects ◽  
Mouth Pressure ◽  
End Tidal ◽  
Visual Analogue Scaling ◽  
The Brain ◽  
Normal Adults

To clarify whether endogenous opioids modulate the dyspnea intensity and, if so, by what mechanism they act on it, we examined 12 healthy male volunteers aged 19–27 yr for ventilatory and peak mouth pressure (Pm) responses to hypoxic progressive hypercapnia with inspiratory flow-resistive loading after the intravenous infusion of 3 mg of naloxone or saline. The intensity of dyspnea was simultaneously assessed by visual analogue scaling every 15 s. Naloxone administration increased both ventilatory and Pm responses to hypoxic progressive hypercapnia (P < 0.05 for both). The increase in dyspnea intensity for a given increase in end-tidal PCO2 was significantly greater after naloxone infusion than after saline (P < 0.05). However, there were no differences in the increase in dyspnea intensity for a given increase in minute ventilation or Pm. These results suggest that the endogenous opioid system suppresses the respiratory output under a strong, acute respiratory stress in normal adults and that this system may relieve the dyspnea sensation secondary to the suppression of the brain stem respiratory center without specific effects on the processing of respiratory sensations in the higher brain.

Effect of progesterone on the activation of neurones of the supraoptic nucleus during parturition

Reproduction ◽  
2000 ◽  
pp. 367-376 ◽  
Author(s):  
IA Antonijevic ◽  
JA Russell ◽  
RJ Bicknell ◽  
G Leng ◽  
AJ Douglas
Keyword(s):  
Progesterone Receptor ◽  
Supraoptic Nucleus ◽  
Late Pregnancy ◽  
Endogenous Opioids ◽  
Opioid Antagonist ◽  
Endogenous Opioid ◽  
Fos Expression ◽  
Oxytocin Neurones ◽  
Supraoptic Nuclei

Parturition is driven by a pulsatile pattern of oxytocin secretion, resulting from burst firing activity of supraoptic oxytocin neurones and reflected by induction of Fos expression. Rats were injected with progesterone on day 20 of pregnancy to investigate the role of the decreasing progesterone:ratio oestrogen ratio, which precedes delivery, in the activation of supraoptic neurones. Progesterone delayed the onset of birth by 28 h compared with vehicle (control) and prolonged the duration of delivery, which was overcome by pulsatile injections of oxytocin, indicating that the slow delivery may reflect impaired oxytocin secretion. Parturient rats pretreated with progesterone had fewer Fos immunoreactive nuclei in the supraoptic nucleus than did parturient rats pretreated with vehicle. The number of Fos immunoreactive nuclei was not restored after oxytocin injection, indicating that appropriate activation of oxytocin neurones is impaired by progesterone and also that there is a lack of stimulatory afferent drive. Fos expression increased in the nucleus of the tractus solitarius during parturition in rats pretreated with either vehicle or progesterone, but not in rats that had been pretreated with progesterone and induced with oxytocin, indicating that this input was inhibited. Endogenous opioids inhibit oxytocin neurones in late pregnancy and the opioid antagonist, naloxone, increases Fos expression in supraoptic nuclei by preventing inhibition. However, progesterone attenuated naloxone-induced Fos expression in the supraoptic nucleus in late pregnancy and naloxone administered during parturition did not accelerate the duration of births delayed by progesterone administration, indicating that progesterone does not act by hyperactivation of endogenous opioid tone. RU486, a progesterone receptor antagonist, enhanced supraoptic neurone Fos expression in late pregnancy, indicating progesterone receptor-mediated actions. Thus, progesterone withdrawal is necessary for appropriate activation of supraoptic and tractus solitarius neurones during parturition.

Stress activates pronociceptive endogenous opioid signalling in DRG neurons during chronic colitis

Gut ◽  
2016 ◽  
Vol 66 (12) ◽  
pp. 2121-2131 ◽  
Author(s):  
Raquel Guerrero-Alba ◽  
Eduardo E Valdez-Morales ◽  
Nestor N Jimenez-Vargas ◽  
Cintya Lopez-Lopez ◽  
Josue Jaramillo-Polanco ◽  
...  
Keyword(s):  
G Protein ◽  
Imaging Techniques ◽  
Stress Hormones ◽  
Endogenous Opioids ◽  
Opioid Use ◽  
Chronic Colitis ◽  
Drg Neurons ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Stress Changes

Aims and backgroundPsychological stress accompanies chronic inflammatory diseases such as IBD, and stress hormones can exacerbate pain signalling. In contrast, the endogenous opioid system has an important analgesic action during chronic inflammation. This study examined the interaction of these pathways.MethodsMouse nociceptive dorsal root ganglia (DRG) neurons were incubated with supernatants from segments of inflamed colon collected from patients with chronic UC and mice with dextran sodium sulfate (cDSS)-induced chronic colitis. Stress effects were studied by adding stress hormones (epinephrine and corticosterone) to dissociated neurons or by exposing cDSS mice to water avoidance stress. Changes in excitability of colonic DRG nociceptors were measured using patch clamp and Ca2+imaging techniques.ResultsSupernatants from patients with chronic UC and from colons of mice with chronic colitis caused a naloxone-sensitive inhibition of neuronal excitability and capsaicin-evoked Ca2+responses. Stress hormones decreased signalling induced by human and mouse supernatants. This effect resulted from stress hormones signalling directly to DRG neurons and indirectly through signalling to the immune system, leading to decreased opioid levels and increased acute inflammation. The net effect of stress was a change endogenous opioid signalling in DRG neurons from an inhibitory to an excitatory effect. This switch was associated with a change in G protein-coupled receptor excitatory signalling to a pathway sensitive to inhibitors of protein kinase A-protein, phospholipase C-protein and G protein βϒ subunits.ConclusionsStress hormones block the inhibitory actions of endogenous opioids and can change the effect of opioid signalling in DRG neurons to excitation. Targeting these pathways may prevent heavy opioid use in IBD.

Opioid peptides and testicular activity in the lizard Podarcis s. sicula Raf

1994 ◽  
Vol 143 (3) ◽  
pp. 565-571 ◽  
Author(s):  
G Ciarcia ◽  
F Facchinetti ◽  
M Vallarino ◽  
M Pestarino ◽  
M Paolucci ◽  
...  
Keyword(s):  
Opioid Peptides ◽  
High Performance ◽  
Physiological Role ◽  
Reproductive Activity ◽  
Opioid System ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Naltrexone Treatment

Abstract In mammals endorphinergic systems have been shown to modulate reproductive processes and β-endorphin (β-EP) has been found to influence sexual functions, acting at the hypothalamus-pituitary-gonadal axis level. Using immunocytochemical and in vitro studies, evidence for a diffuse pro-opiomelanocortin-related opioid system in the lizard Podarcis s. sicula was produced. In the testis, β-EP immunoreactivity showed seasonal variation, being most pronounced in the interstitial cells of sexually quiescent lizards (December). Reverse-phase high-performance liquid chromatography, coupled with radioimmunoassay and immunocytochemistry, showed that β-EP and acetyl β-EP increased during December, while their concentrations were low during April, when the highest testicular activity occurred. Using in vivo studies, it was found that naltrexone treatment, blocking pituitary opioid receptor, increased androgen levels in the plasma and in the testis. It was also found with in vitro studies that the endogenous opioid system inhibits gonadotrophin release and therefore androgen production by the testis. The data reported here provide evidence for the physiological role played by opioid peptides at the pituitary level to regulate the seasonal reproductive activity of the lizard Podarcis s. sicula. Journal of Endocrinology (1994) 143, 565–571

scholarly journals ENDOGENOUS OPIOID SYSTEM AS A MEDIATOR OF ACUTE AND LONG-TERM ADAPTATION TO STRESS. PROSPECTS FOR CLINICAL USE OF OPIOID PEPTIDES

2012 ◽  
Vol 67 (6) ◽  
pp. 73-82 ◽  
Author(s):  
Yu. B. Lishmanov ◽  
L. N. Maslov ◽  
N. Yu. Naryzhnaya ◽  
J.-M. Pei ◽  
F. Kolar ◽  
...  
Keyword(s):  
Opioid Peptides ◽  
Ischemia Reperfusion ◽  
Antiarrhythmic Effect ◽  
Endogenous Opioids ◽  
Protective Effects ◽  
Adaptive Responses ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Future Clinical Practice ◽  
Thromboxane Production

It has been well established that opioid peptides (OPs) affect various hormonal systems. Opioids exhibit stress-limiting and gastro-protective effects in stressed animals, acting via μ- and δ-opioid receptors (OR). Peripheral μ-OR stimulation by endogenous and exogenous opioids increases cardiac tolerance to pathological consequences of stress. Enhancement of prostacyclin synthesis, decrease of thromboxane production as well as suppression of lipid peroxidation can be directly responsible for cardioprotective effects of OPs in stressed animals. Adaptive responses are accompanied by increased OP levels in blood and tissues. Reduction of ventricular arrhythmias induced by repeated short-term immobilization stress is mediated via μ-OR stimulation by endogenous opioids, while δ-OR account for an antiarrhythmic effect of adaptation to chronic intermittent hypobaric hypoxia. The mechanism of infarct size-limiting effect of continuous normobaric hypoxia involves both μ- and δ-OR stimulation. Peptide OR agonists can be considered in future clinical practice for treatment of withdrawal syndrome, stress-related cardiac disease or myocardial injury caused by ischemia-reperfusion insult. 

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