Propranolol and the treatment of rheumatoid arthritis

Kaplan, Roy A.; Robinson, C A; Scavulli, John F.; Vaughan, John H.

doi:10.1002/art.1780230220

Cited by 39 publications

(22 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Additionally, chronic administration of β-adrenergic receptor (βAR) agonists produces a painful arthritis-like syndrome (Vyden et al 1971). These findings are consistent with clinical observations that sympathetic blockade or administration of the βAR antagonist propranolol reduces the severity of arthritis and joint responses to injury (Baerwald et al 1997;Kaplan et al 1980;Levine et al 1986b).…”

Section: Nih-pa Author Manuscriptsupporting

confidence: 57%

Catechol- O -methyltransferase inhibition increases pain sensitivity through activation of both β2- and β3-adrenergic receptors

Nackley

Tan

Fecho

et al. 2007

Pain

258

200

View full text Add to dashboard Cite

Catechol-O-methyltransferase (COMT), an enzyme that metabolizes catecholamines, has recently been implicated in the modulation of pain. Our group demonstrated that human genetic variants of COMT are predictive for the development of Temporomandibular Joint Disorder (TMJD) and are associated with heightened experimental pain sensitivity (Diatchenko et al. 2005). Variants associated with heightened pain sensitivity produce lower COMT activity. Here we report the mechanisms underlying COMT-dependent pain sensitivity. To characterize the means whereby elevated catecholamine levels, resulting from reduced COMT activity, modulate heightened pain sensitivity, we administered a COMT inhibitor to rats and measured behavioral responsiveness to mechanical and thermal stimuli. We show that depressed COMT activity results in enhanced mechanical and thermal pain sensitivity. This phenomenon is completely blocked by the nonselective β-adrenergic antagonist propranolol or by the combined administration of selective β 2 -and β 3 -adrenergic antagonists, while administration of β 1 -adrenergic, α-adrenergic, or dopaminergic receptor antagonists fail to alter COMT-dependent pain sensitivity. These data provide the first direct evidence that low COMT activity leads to increased pain sensitivity via a β 2/3 -adrenergic mechanism. These findings are of considerable clinical importance, suggesting that pain conditions resulting from low COMT activity and/or elevated catecholamine levels can be treated with pharmacological agents that block both β 2 -and β 3 -adrenergic receptors. Keywords epinephrine; norepinephrine; catecholamines; allodynia; hyperalgesia; carrageenan Catecholamines and enzymatic pathways that regulate the bioavailability of catecholamines influence persistent pain. Adrenergic systems contribute to the pathogenesis of rheumatoid Corresponding Author: Andrea G Neely, Center for Neurosensory Disorders, School of Dentistry, CB 7450, University of North Carolina, Chapel Hill, NC 27599-7450, Phone: (919) 966-2953, Fax: (919) Email: andrea_nackley@dentistry.unc.edu Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptPain. Author manuscript; available in PMC 2007 July 2. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript arthritis in animals, as denervation of sympathetic noradrenergic fibers (Levine et al. 1986a) and depletion of peripheral epinephrine (Coderre et al. 1990) attenuate arthritic responses. Additionally, chronic administration of β-adrenergic receptor (βAR) agonists produces a painful arthritis-like s...

show abstract

Section: Nih-pa Author Manuscriptsupporting

confidence: 57%

Catechol- O -methyltransferase inhibition increases pain sensitivity through activation of both β2- and β3-adrenergic receptors

Nackley

Tan

Fecho

et al. 2007

Pain

258

200

View full text Add to dashboard Cite

show abstract

“…4 Data obtained by our group demonstrated that the peripheral antinociceptive effect of the adrenoceptor agonist xylazine involves the activation of α 2C adrenoreceptor 5 thus inducing nitric oxide synthase to produce nitric oxide with a subsequent increase of cyclic guanosine monophosphate in peripheral nociceptors 6 and opening of adenosine triphosphate-sensitive K + channels. 7 Activation of the β adrenoceptor is responsible for analgesia in patients with rheumatoid arthritis 8 and in rats with adjuvant-induced arthritis. 9,10 In addition, norepinephrine injected directly into inflamed rat hindpaw, via immune cells participation, produced dose-dependent antinociception, blocked by α 1 , α 2 , and β 2 adrenoceptor antagonists.…”

mentioning

confidence: 99%

CB1 and CB2 Cannabinoid Receptor Agonists Induce Peripheral Antinociception by Activation of the Endogenous Noradrenergic System

Romero

Resende²,

Guzzo³

et al. 2013

Anesthesia &Amp; Analgesia

View full text Add to dashboard Cite

show abstract

“…17,31,37,[39][40][41] Although in most experiments the role of norepinephrine 1,12,24,26,28,40,43,44 was evaluated, recent behavioral studies have shown that epinephrine (EPI) also produces mechanical hyperalgesia. 20,29 Because ␤-adrenergic receptor antagonists can attenuate rheumatoid arthritis pain in human beings 27 and adjuvant-induced arthritis in rats, 32 it is possible that EPI plays a role in those inflammatory pain states. 30 In spite of this, there have been very few electrophysiologic studies of the effect of EPI on primary afferent nociceptors.…”

mentioning

confidence: 99%