ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2002
Local injection of a selective endothelin-B receptor agonist inhibits endothelin-1-induced pain-like behavior and excitation of nociceptors in a naloxone-sensitive manner.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 72 citations in OpenAlex.
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- Longitudinal peripheral tissue RNA-Seq transcriptomic profiling, hyperalgesia, and wound healing in the rat plantar surgical incision model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Longitudinal Transcriptomic Profiling in Carrageenan-Induced Rat Hind Paw Peripheral Inflammation and Hyperalgesia Reveals Progressive Recruitment of Innate Immune System Components.The journal of pain · 2021Article
- Role of central endothelin-1 in hyperalgesia, anhedonia, and hypolocomotion induced by endotoxin in male rats.Experimental brain research · 2021Article
- Lifting the veil on the keratinocyte contribution to cutaneous nociception.Protein & cell · 2020Review
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- Endothelin-1 Decreases Excitability of the Dorsal Root Ganglion Neurons via ETMolecular neurobiology · 2018Article
- Bosentan, a mixed endothelin receptor antagonist, inhibits superoxide anion-induced pain and inflammation in mice.Naunyn-Schmiedeberg's archives of pharmacology · 2015Article
- Intradermal endothelin-1 excites bombesin-responsive superficial dorsal horn neurons in the mouse.Journal of neurophysiology · 2015Article
- Molecular and cellular mechanisms that initiate pain and itch.Cellular and molecular life sciences : CMLS · 2015Review
- Role of renal sensory nerves in physiological and pathophysiological conditions.American journal of physiology. Regulatory, integrative and comparative physiology · 2015Review
- Effect of short-term hyperinsulinemia on the localization and expression of endothelin receptors A and B in lamellar tissue of the forelimbs of horses.American journal of veterinary research · 2014Article
- Evidence for the endothelin system as an emerging therapeutic target for the treatment of chronic pain.Journal of pain research · 2014Review
- Progressive endothelin-1 gene activation initiates chronic/end-stage renal disease following experimental ischemic/reperfusion injury.Kidney international · 2013Article
- Biologic mechanisms of oral cancer pain and implications for clinical therapy.Journal of dental research · 2012Review
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- Endogenous endothelin stimulates cardiac sympathetic afferents during ischaemia.The Journal of physiology · 2010Article
- Mechanism of cancer pain.Molecular interventions · 2010Review
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Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
We showed previously that subcutaneous injection of the injury-associated peptide mediator endothelin-1 (ET-1) into the rat plantar hindpaw produces pain behavior and selective excitation of nociceptors, both through activation of ET(A) receptors likely on nociceptive terminals. The potential role of ET(B) receptor activation in these actions of ET-1-has not been examined. Therefore, in these experiments, we studied the effect of blocking or activating ET(B) receptors on ET-1-induced hindpaw flinching and excitation of nociceptors in rats. An ET(B) receptor-selective antagonist, BQ-788 (3 mm), coinjected with ET-1 (200 microm) reduced the time-to-peak of flinching and significantly enhanced the average maximal flinch frequency (MFF). In contrast, coinjection of an ET(B) receptor selective agonist, IRL-1620 (100 or 200 microm), with ET-1 reduced the average MFF and the average total number of flinches. Interestingly, this unexpected inhibitory effect of IRL-1620 was prevented by the nonselective opioid receptor antagonist naloxone (2.75 mm). To confirm these inhibitory actions, we studied the effects of IRL-1620 on ET-1-induced spike responses in single, physiologically characterized nociceptive C-fibers. IRL-1620 suppressed spike responses to ET-1 in all (n = 12) C-units, with mean and maximum response frequencies of 0.08 +/- 0.02 and 1.5 +/- 0.4 impulses/sec versus 0.32 +/- 0.07 and 4.17 +/- 0.17 impulses/sec for ET-1 alone. In additional support of the behavioral results, coinjection of naloxone (2.75 mm) completely prevented this inhibitory action of IRL-1620. These results establish that ET(B) receptor activation inhibits ET-1-induced pain behavior and nociception in a naloxone-sensitive manner and point to a previously unrecognized dual modulation of acute nociceptive signaling by ET(A) and ET(B) receptors in cutaneous tissues.
Indexed as
Identifiers
12196602PMC6757974W1945577104What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.