Preemptive analgesia by zaltoprofen that inhibits bradykinin action and cyclooxygenase in a post-operative pain model

Muratani, Tadatoshi; Doi, Yumi; Nishimura, Wataru; Nishizawa, Mikio; Minami, Toshiaki; Ito, Seiji

doi:10.1016/j.neures.2004.12.010

Cited by 21 publications

(16 citation statements)

References 20 publications

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“…HOE 140 was also injected in another group of animals 30 min after exercise. These antagonists are receptor specific (Hock et al, 1991;Wirth et al, 1991), and the dosages used are sufficient to antagonize bradykinin in a postoperative pain model (Muratani et al, 2005) and inflamed conditions (Fox et al, 2003).…”

Section: Drugs Calculation Of Percentage Suppression Of Hyperalgesiamentioning

confidence: 99%

Bradykinin and Nerve Growth Factor Play Pivotal Roles in Muscular Mechanical Hyperalgesia after Exercise (Delayed-Onset Muscle Soreness)

Murase

Terazawa²,

Queme³

et al. 2010

J. Neurosci.

160

183

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Unaccustomed strenuous exercise that includes lengthening contraction (LC) often causes delayed-onset muscle soreness (DOMS), a kind of muscular mechanical hyperalgesia. The substances that induce this phenomenon are largely unknown. Peculiarly, DOMS is not perceived during and shortly after exercise, but rather is first perceived after ϳ1 d. Using B 2 bradykinin receptor antagonist HOE 140, we show here that bradykinin released during exercise plays a pivotal role in triggering the process that leads to muscular mechanical hyperalgesia. HOE 140 completely suppressed the development of muscular mechanical hyperalgesia when injected before LC, but when injected 2 d after LC failed to reverse mechanical hyperalgesia that had already developed. B 1 antagonist was ineffective, regardless of the timing of its injection. Upregulation of nerve growth factor (NGF) mRNA and protein occurred in exercised muscle over a comparable time course (12 h to 2 d after LC) for muscle mechanical hyperalgesia. Antibodies to NGF injected intramuscularly 2 d after exercise reversed muscle mechanical hyperalgesia. HOE 140 inhibited the upregulation of NGF. In contrast, shortening contraction or stretching induced neither mechanical hyperalgesia nor NGF upregulation. Bradykinin together with shortening contraction, but not bradykinin alone, reproduced lasting mechanical hyperalgesia. We also showed that rat NGF sensitized thin-fiber afferents to mechanical stimulation in the periphery after 10 -20 min. Thus, NGF upregulation through activation of B 2 bradykinin receptors is essential (though not satisfactory) to mechanical hyperalgesia after exercise. The present observations explain why DOMS occurs with a delay, and why lengthening contraction but not shortening contraction induces DOMS.

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Section: Drugs Calculation Of Percentage Suppression Of Hyperalgesiamentioning

confidence: 99%

Bradykinin and Nerve Growth Factor Play Pivotal Roles in Muscular Mechanical Hyperalgesia after Exercise (Delayed-Onset Muscle Soreness)

Murase

Terazawa²,

Queme³

et al. 2010

J. Neurosci.

160

183

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“…Plantar incision-induced mechanical hyperalgesia was reduced by pretreatment with icatibant, but not des-Arg 10 -HOE-140, from 2 h to 3 days post surgery in mice (520). The enhanced bradykinin responsiveness of cutaneous nociceptors in the inflamed isolated skin from CFA-pretreated rats was exclusively mediated by B 2 receptors (39).…”

mentioning

confidence: 99%

Sensory and Signaling Mechanisms of Bradykinin, Eicosanoids, Platelet-Activating Factor, and Nitric Oxide in Peripheral Nociceptors

Pethő

Reeh

2012

Physiological Reviews

240

200

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Peripheral mediators can contribute to the development and maintenance of inflammatory and neuropathic pain and its concomitants (hyperalgesia and allodynia) via two mechanisms. Activation or excitation by these substances of nociceptive nerve endings or fibers implicates generation of action potentials which then travel to the central nervous system and may induce pain sensation. Sensitization of nociceptors refers to their increased responsiveness to either thermal, mechanical, or chemical stimuli that may be translated to corresponding hyperalgesias. This review aims to give an account of the excitatory and sensitizing actions of inflammatory mediators including bradykinin, prostaglandins, thromboxanes, leukotrienes, platelet-activating factor, and nitric oxide on nociceptive primary afferent neurons. Manifestations, receptor molecules, and intracellular signaling mechanisms of the effects of these mediators are discussed in detail. With regard to signaling, most data reported have been obtained from transfected nonneuronal cells and somata of cultured sensory neurons as these structures are more accessible to direct study of sensory and signal transduction. The peripheral processes of sensory neurons, where painful stimuli actually affect the nociceptors in vivo, show marked differences with respect to biophysics, ultrastructure, and equipment with receptors and ion channels compared with cellular models. Therefore, an effort was made to highlight signaling mechanisms for which supporting data from molecular, cellular, and behavioral models are consistent with findings that reflect properties of peripheral nociceptive nerve endings. Identified molecular elements of these signaling pathways may serve as validated targets for development of novel types of analgesic drugs.

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“…The NSAID zaltoprofen [1][2][3][4] exerts anti-inflammatory actions by inhibiting prostaglandin synthesis and also inhibits bradykinin-induced pain and is widely used for e.g. rheumatoid arthritis, osteoarthritis, low back pain and other inflammatory pain syndromes in Japan.…”

Section: Introductionmentioning

confidence: 99%

A Double-Blind Study of Zaltoprofen for the Treatment of Upper Respiratory Tract Infection

Azuma¹,

Kudoh²,

Nakashima³

et al. 2009

Pharmacology

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We conducted a double-blind study to evaluate the antipyretic and analgesic effects of a single administration of zaltoprofen, a nonsteroidal anti-inflammatory drug, in patients with acute upper respiratory tract infection. 170 patients were assigned to one of the 3 treatment groups (80, 160 mg, placebo). Changes over time of body temperature and the visual analog scale score of pain were measured under the supervision of the study staff at the participating medical institutions. A significant decrease in body temperature from the baseline value was noted at all measurement points from 0.5 to 6 h after drug administration in the zaltoprofen groups. The lowest temperature during the observation period was recorded between 3 and 4 h, and the body temperature tended to rise at 6 h. No significant decrease in body temperature was noted at any time during the observation period in the placebo group. A significant decrease in pain scores from the baseline was noted at all measurement points in the zaltoprofen groups, and the decrease was maintained even at 6 h. An analgesic effect but no antipyretic effect was observed in the placebo group.

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Preemptive analgesia by zaltoprofen that inhibits bradykinin action and cyclooxygenase in a post-operative pain model

Cited by 21 publications

References 20 publications

Bradykinin and Nerve Growth Factor Play Pivotal Roles in Muscular Mechanical Hyperalgesia after Exercise (Delayed-Onset Muscle Soreness)

Bradykinin and Nerve Growth Factor Play Pivotal Roles in Muscular Mechanical Hyperalgesia after Exercise (Delayed-Onset Muscle Soreness)

Sensory and Signaling Mechanisms of Bradykinin, Eicosanoids, Platelet-Activating Factor, and Nitric Oxide in Peripheral Nociceptors

A Double-Blind Study of Zaltoprofen for the Treatment of Upper Respiratory Tract Infection

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