Amelioration of hyperalgesia by kinin receptor antagonists or kininogen deficiency in chronic constriction nerve injury in rats

Yamaguchi-Sase, S.; Hayashi, Izumi; Okamoto, Hirotsugu; Nara, Yoshihiro; Matsuzaki, Shigeyuki; Hoka, Sumio; Murakami, Masataka

doi:10.1007/s000110300067

Cited by 28 publications

(31 citation statements)

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“…Increased levels of B 1 and B 2 receptor mRNA or protein have been found in dorsal root ganglia (DRGs) after sciatic nerve constriction in rats and mice (Petersen et al, 1998;Eckert et al, 1999;Levy and Zochodne, 2000;Yamaguchi-Sase et al, 2003;Rashid et al, 2004). Of note, the systemic administration of B 1 or B 2 receptor antagonists has been found to reduce thermal hyperalgesia and mechanical allodynia produced by sciatic nerve constriction in rats (Levy and Zochodne, 2000;Yamaguchi-Sase et al, 2003;Gougat et al, 2004). Plasma seems to be the main source of endogenous kinins after nerve injury, and there is recent evidence demonstrated that neuropathic pain is reduced in mutant plasma kininogen-deficient B/N-Katholiek rats when compared with normal B/N-Kitasato rats (Yamaguchi-Sase et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

“…Of note, the systemic administration of B 1 or B 2 receptor antagonists has been found to reduce thermal hyperalgesia and mechanical allodynia produced by sciatic nerve constriction in rats (Levy and Zochodne, 2000;Yamaguchi-Sase et al, 2003;Gougat et al, 2004). Plasma seems to be the main source of endogenous kinins after nerve injury, and there is recent evidence demonstrated that neuropathic pain is reduced in mutant plasma kininogen-deficient B/N-Katholiek rats when compared with normal B/N-Kitasato rats (Yamaguchi-Sase et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

“…B 1 receptor mRNA and protein are constitutively expressed in mouse, rat, and monkey DRG (Seabrook et al, 1997;Levy and Zochodne, 2000;Ma et al, 2000;Wotherspoon and Winter, 2000;Shughrue et al, 2003;Yamaguchi-Sase et al, 2003;Rashid et al, 2004). B 1 receptors are predominantly expressed by small-diameter DRG neurons colocalized with isolectin B4 and calcitonin gene-related peptide that are contained in C and A␦ fibers (Ma, 2001).…”

Section: Discussionmentioning

confidence: 99%

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Reduced Nerve Injury-Induced Neuropathic Pain in Kinin B₁Receptor Knock-Out Mice

Ferreira¹,

Beirith²,

Mori³

et al. 2005

J. Neurosci.

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Injury to peripheral nerves often results in a persistent neuropathic pain condition that is characterized by spontaneous pain, allodynia, and hyperalgesia. Nerve injury is accompanied by a local inflammatory reaction in which nerve-associated and immune cells release several pronociceptive mediators. Kinin B 1 receptors are rarely expressed in nontraumatized tissues, but they can be expressed after tissue injury. Because B 1 receptors mediate chronic inflammatory painful processes, we studied their participation in neuropathic pain using receptor gene-deleted mice. In the absence of neuropathy, we found no difference in the paw-withdrawal responses to thermal or mechanical stimulation between B 1 receptor knock-out mice and 129/J wild-type mice. Partial ligation of the sciatic nerve in the wild-type mouse produced a profound and long-lasting decrease in thermal and mechanical thresholds in the paw ipsilateral to nerve lesion.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Reduced Nerve Injury-Induced Neuropathic Pain in Kinin B₁Receptor Knock-Out Mice

Ferreira¹,

Beirith²,

Mori³

et al. 2005

J. Neurosci.

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“…Although it is unknown whether endogenous bradykinin is involved in the development and/or maintenance of neuropathic pain, its release from injured tissue site as well as the inhibition of neuropathic hyperalgesia by its receptor blockade (Levy and Zochodne, 2000;Yamaguchi-Sase et al, 2003) indicate its role in neuropathic pain following nerve injury. In this report, we showed that exogenous application of very low doses of BK at the peripheral nerve endings in mice produced potent nociceptive flexion response, and these responses were sensitized after peripheral nerve injury.…”

Section: Discussionmentioning

confidence: 99%

Switching of Bradykinin-Mediated Nociception Following Partial Sciatic Nerve Injury in Mice

Rashid¹,

Inoue²,

Matsumoto³

et al. 2003

J Pharmacol Exp Ther

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Bradykinin (BK) is well known as a potent mediator of pain and hyperalgesia. Using a highly sensitive nociception test, we found that intraplantar (i.pl.) injection of BK produced nociceptive hyper-responses in partial sciatic nerve-injured mice, compared with the control sham-operated animals. By use of selective agonists and antagonists, we revealed that BK nociception in sham-operated mice was mediated through B2 receptor, whereas that in injured mice was mediated through B1 receptor. When we examined the activation of extracellular signal-regulated protein kinase (ERK) in dorsal root ganglion (DRG) neurons upon i.pl. injection of BK, phosphorylated ERK was mainly observed in unmyelinated neurons in sham-operated mice, and in case of nerve-injured mice, ERK was mainly activated in myelinated neurons and satellite cells. The B1 receptor agonist, [Lys-des-Arg 9 ]-BK also produced nociceptive response and activated ERK only in nerve-injured mice. BK or B1 agonist-induced activation of ERK in DRG neurons of nerveinjured mice was completely blocked by pretreatment with antisense oligodeoxynucleotide (AS-ODN) for B1 receptor. We found that in sham-operated mice mainly B2 receptors were expressed in unmyelinated DRG neurons with a very little presence of B1 receptor. After nerve injury, B2 receptor expression drastically decreased, whereas B1 receptors were newly expressed mainly in myelinated DRG neurons and satellite cells. Finally, BK nociception in sham-operated mice was blocked by AS-ODN for B2 receptors and that in injured mice by AS-ODN for B1 receptors. Altogether, these findings confirm a switching of receptor and fiber subtype for BK nociception after peripheral nerve injury, which might contribute to the pathobiology of neuropathic pain.Traumatic nerve injury is often associated with local inflammation of the injured nerve and release of proinflammatory mediators including bradykinin, prostaglandins, tumor necrosis factor-␣, interleukin-1␤, etc. It has been proposed that the local release of such proinflammatory mediators might play a critical role in the development and maintenance of neuropathic pain (Bennett 1999;Cui et al., 2000;Schafers et al., 2003). The nonapeptide bradykinin is one of the most potent among the proinflammatory mediators and is produced from plasma globulin kininogens by action of specific enzyme kallikreins (Bhoola et al., 1992). It participates in processes such as tissue permeability, vascular dilation, smooth muscle contraction, and sensory nerve-ending stimulation (Regoli and Barabe 1980;Bhoola et al., 1992). Since the kallikreins are normally present in their inactive forms, only a small amount of bradykinin is present in the plasma and tissues under normal physiological conditions (Bhoola et al., 1992). After tissue injury, kallikreins are activated, and bradykinin is released from damaged tissue and mediates pain and hyperalgesia (Bhoola et al., 1992;Calixto et al., 2000).Upon release, bradykinin exerts its physiological effects through activation of two pharmacologi...

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“…This increase included a de novo expression of B 1 receptors and an enhancement of the density of preexisting B 2 receptors, and it was accompanied by an increase in the number of bradykinin binding sites on individual neurons. Chronic constriction injury (CCI) to the rat sciatic nerve led to similar changes: an increased B 2 receptor mRNA expression on day 2 and a marked increase in preexisting B 1 receptor mRNA expression 14 day after surgery (428,784). Following crush injury of the sciatic nerve in mice, B 2 receptor mRNA level was elevated in DRG neurons peaking on day 7, and this upregulation was due to an increase in the mRNA content of the neurons (412).…”

Section: Role Of Bradykinin Receptors In Neuropathic Hyperalgesiamentioning

confidence: 95%

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

Pethő

Reeh

2012

Physiological Reviews

244

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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Amelioration of hyperalgesia by kinin receptor antagonists or kininogen deficiency in chronic constriction nerve injury in rats

Abstract: These data suggests that kinin were at least partly involved in yielding nociceptor hypersensitivity up to day 14 after CCI. Bradykinin and its B1 and B2 receptors were involved in the maintenance of hyperalgesia.

Cited by 28 publications

References 32 publications

Reduced Nerve Injury-Induced Neuropathic Pain in Kinin B₁Receptor Knock-Out Mice

Reduced Nerve Injury-Induced Neuropathic Pain in Kinin B₁Receptor Knock-Out Mice

Switching of Bradykinin-Mediated Nociception Following Partial Sciatic Nerve Injury in Mice

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

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Amelioration of hyperalgesia by kinin receptor antagonists or kininogen deficiency in chronic constriction nerve injury in rats

Abstract: These data suggests that kinin were at least partly involved in yielding nociceptor hypersensitivity up to day 14 after CCI. Bradykinin and its B1 and B2 receptors were involved in the maintenance of hyperalgesia.

Cited by 28 publications

References 32 publications

Reduced Nerve Injury-Induced Neuropathic Pain in Kinin B1Receptor Knock-Out Mice

Reduced Nerve Injury-Induced Neuropathic Pain in Kinin B1Receptor Knock-Out Mice

Switching of Bradykinin-Mediated Nociception Following Partial Sciatic Nerve Injury in Mice

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

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Reduced Nerve Injury-Induced Neuropathic Pain in Kinin B₁Receptor Knock-Out Mice

Reduced Nerve Injury-Induced Neuropathic Pain in Kinin B₁Receptor Knock-Out Mice