Peripheral nitric oxide signaling directly blocks inflammatory pain

[Display omitted] Pain is a classical sign of inflammation, and sensitization of primary sensory neurons (PSN) is the most important mediating mechanism. This mechanism involves direct action of inflammatory mediators such as prostaglandins and sympathetic amines. Pharmacologic control of inflammato...

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Bibliographic Details
Published in:Biochemical pharmacology Vol. 176; p. 113862
Main Authors: Gomes, Francisco Isaac F., Cunha, Fernando Q., Cunha, Thiago M.
Format: Journal Article
Language:English
Published: England Elsevier Inc 01.06.2020
Subjects:
Analgesia
Inflammatory pain
Nitric oxide
Nociception
PI3Kgamma
eNOS
GTP
ACh
K+ATP
CXCL1
TNF
sGC
iNOS
ODQ
PKGI and PKGII
L-NAME
TRPV
NKA
NOARG
IL1β
PSN
PI3Kγ
PPARγ
CB1
EDRF
Nitric oxide
L-NIO
nNOS
GPCR
KT5823
L-NMMA
CGRP
Inflammatory pain
NPA
NO
A1R
L-NNA
cGMP
cAMP
DPDPE
LPS
NSAIDs
PI3Kgamma
Nociception
PGE2
NaV
HMG-CoA
AKT
SNAP
Analgesia
IL6
TG
CPA
DRG
ISSN:0006-2952, 1873-2968, 1873-2968
Online Access:Get full text
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Summary:[Display omitted] Pain is a classical sign of inflammation, and sensitization of primary sensory neurons (PSN) is the most important mediating mechanism. This mechanism involves direct action of inflammatory mediators such as prostaglandins and sympathetic amines. Pharmacologic control of inflammatory pain is based on two principal strategies: (i) non-steroidal anti-inflammatory drugs targeting inhibition of prostaglandin production by cyclooxygenases and preventing nociceptor sensitization in humans and animals; (ii) opioids and dipyrone that directly block nociceptor sensitization via activation of the NO signaling pathway. This review summarizes basic concepts of inflammatory pain that are necessary to understand the mechanisms of peripheral NO signaling that promote peripheral analgesia; we also discuss therapeutic perspectives based on the modulation of the NO pathway.
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ISSN:0006-2952
1873-2968
1873-2968
DOI:10.1016/j.bcp.2020.113862