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. 

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 Reward Processing by the Opioid System in the Brain

2009 ◽  
Vol 89 (4) ◽  
pp. 1379-1412 ◽  
Author(s):  
Julie Le Merrer ◽  
Jérôme A. J. Becker ◽  
Katia Befort ◽  
Brigitte L. Kieffer
Keyword(s):  
Opioid Peptides ◽  
Drugs Of Abuse ◽  
Gene Knockout ◽  
Reward Processing ◽  
Endogenous Opioids ◽  
Therapeutic Interventions ◽  
Opioid System ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Addictive Disorders

The opioid system consists of three receptors, mu, delta, and kappa, which are activated by endogenous opioid peptides processed from three protein precursors, proopiomelanocortin, proenkephalin, and prodynorphin. Opioid receptors are recruited in response to natural rewarding stimuli and drugs of abuse, and both endogenous opioids and their receptors are modified as addiction develops. Mechanisms whereby aberrant activation and modifications of the opioid system contribute to drug craving and relapse remain to be clarified. This review summarizes our present knowledge on brain sites where the endogenous opioid system controls hedonic responses and is modified in response to drugs of abuse in the rodent brain. We review 1) the latest data on the anatomy of the opioid system, 2) the consequences of local intracerebral pharmacological manipulation of the opioid system on reinforced behaviors, 3) the consequences of gene knockout on reinforced behaviors and drug dependence, and 4) the consequences of chronic exposure to drugs of abuse on expression levels of opioid system genes. Future studies will establish key molecular actors of the system and neural sites where opioid peptides and receptors contribute to the onset of addictive disorders. Combined with data from human and nonhuman primate (not reviewed here), research in this extremely active field has implications both for our understanding of the biology of addiction and for therapeutic interventions to treat the disorder.

Endogenous opioids and ventilatory responses to hypercapnia in normal humans

1985 ◽  
Vol 58 (5) ◽  
pp. 1415-1420 ◽  
Author(s):  
S. E. Weinberger ◽  
R. A. Steinbrook ◽  
D. B. Carr ◽  
E. R. von Gal ◽  
J. E. Fisher ◽  
...  
Keyword(s):  
Opioid Peptides ◽  
Endogenous Opioids ◽  
Opiate Antagonist ◽  
Endogenous Opioid Peptides ◽  
Short Term ◽  
Endogenous Opioid ◽  
Beta Endorphin ◽  
Ventilatory Responses ◽  
Normal Humans

Though administration of opioid peptides depresses ventilation and ventilatory responsiveness, the role of endogenous opioid peptides in modulating ventilatory responsiveness is not clear. We studied the interaction of endogenous opioids and ventilatory responses in 12 adult male volunteers by relating hypercapnic responsiveness to plasma levels of immunoactive beta-endorphin and by administering the opiate antagonist naloxone. Ventilatory responsiveness to hypercapnia was not altered by pretreatment with naloxone, and this by itself suggests that endogenous opioids have no role in modulating this response. However, there was an inverse relationship between basal levels of immunoactive beta-endorphin in plasma and ventilatory responsiveness to CO2. Furthermore, plasma beta-endorphin levels rose after short-term hypercapnia but only when subjects had been pretreated with naloxone. We conclude that measurement of plasma endorphin levels suggests relationships between endogenous opioid peptides and ventilatory responses to CO2 that are not apparent in studies limited to assessing the effect of naloxone.

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 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.

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.

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 Formation of fetal opioid system

2016 ◽  
Vol 65 (2) ◽  
pp. 64-69 ◽  
Author(s):  
Anastasia A Yakovleva
Keyword(s):  
Growth Hormone ◽  
Opioid Peptides ◽  
Opioid System ◽  
Endogenous Opioid Peptides ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Placental Lactogens ◽  
Functional Development ◽  
The Central Nervous System ◽  
Different Tissues

The article presented literature review about of endogenous opioid system (EOS) formation consist of opioid receptors complex and its ligands (endogenous opioid peptides) in different tissues including placenta. It was shown that formation of fetal EOS is going with anatomic and functional development of the central nervous system and EOS expression begins in the placental tissues as soon as implantation and starts till the end of the pregnancy. Influence of opioid peptides on secretion progesterone, prolactin family peptides, growth hormone, placental lactogens and prolypherine from the trophoblast tissue is discussed.

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