Noradrenaline induces peripheral antinociception by endogenous opioid release

The aim of this study was to investigate this involvement in not inflammatory model of pain and which opioid receptor subtype mediates noradrenaline-induced peripheral antinociception. Noradrenaline is involved in the intrinsic control of pain-inducing pro-nociceptive effects in the primary afferent...

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Bibliographic Details
Published in:Pharmacological reports 2018-08, Vol.70 (4), p.784-788
Main Authors: Romero, Thiago Roberto Lima, Soares Santos, Raquel Rodrigues, Castor, Marina Gomes Miranda e, Petrocchi, Júlia Alvarenga, Guzzo, Luciana Souza, Klein, Andre, Duarte, Igor Dimitri Gama
Format: Article
Language:English
Subjects:
Adrenoceptors
Analgesics - pharmacology
Animals
Cinnamates - pharmacology
Dinoprostone
Dose-Response Relationship, Drug
Drug Safety and Pharmacovigilance
Hyperalgesia - chemically induced
Hyperalgesia - prevention & control
Leucine - analogs & derivatives
Leucine - pharmacology
Male
Morphine Derivatives - pharmacology
Naltrexone - analogs & derivatives
Naltrexone - pharmacology
Noradrenaline
Noradrenergic system
Norepinephrine - antagonists & inhibitors
Norepinephrine - pharmacology
Opioid Peptides - metabolism
Original Article
Pain Measurement - drug effects
Peripheral antinociception
Pharmacotherapy
Pharmacy
Prazosin - pharmacology
Propranolol - pharmacology
Rats
Yohimbine - pharmacology
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Summary:The aim of this study was to investigate this involvement in not inflammatory model of pain and which opioid receptor subtype mediates noradrenaline-induced peripheral antinociception. Noradrenaline is involved in the intrinsic control of pain-inducing pro-nociceptive effects in the primary afferent nociceptors. However, inflammation can induce various plastic changes in the central and peripheral noradrenergic system that, upon interaction with the immune system, may contribute, in part, to peripheral antinociception. Hyperalgesia was induced by intraplantar injection of prostaglandin E2 (PGE2, 2μg) into the plantar surface of the right hind paw and the paw pressure test to evaluated the hyperalgesia was used. Noradrenaline (NA) was administered locally into right hind paw of Wistar rat (160–200g) alone and after either agents, α2-adrenoceptor antagonist yohimbine, α1-adrenoceptor antagonist prazosin, β-adrenoceptor antagonist propranolol, μ-opioid antagonist clocinnamox, δ-opioid antagonist naltrindole and κ-opioid antagonist nor-binaltorfimina. In addition, the enkephalinase inhibitor bestatin was administered prior to NA low dose. Intraplantar injection of NA induced peripheral antinociception against hyperalgesia induced by PGE2. This effect was reversed, in dose dependent manner, by intraplantar injection of yohimbine, prazosin, propranolol, clocinnamox and naltrindole. However, injection of nor-binaltorfimina did not alter antinociception of NA after PGE2 hyperalgesia. Bestatin intensified the antinociceptive effects of low-dose of NA. Besides the α2-adrenoceptor, the present data provide evidence that, in absence of inflammation, NA activating α1 and β-adrenoceptor induce endogenous opioid release to produce peripheral antinociceptive effect by μ and δ opioid receptors.
ISSN:1734-1140
2299-5684
DOI:10.1016/j.pharep.2018.02.020