Specific neurokinin receptors mediate plasma extravasation in the rat knee joint

Lam, F.; Ferrell, W.R.

doi:10.1111/j.1476-5381.1991.tb12334.x

Cited by 67 publications

(32 citation statements)

References 24 publications

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“…stimulation (Hagermark et al, 1978;Gamse et al, 1980;Foreman & Jordan, 1984;Foreman, 1987;PedersenBjergaard et al, 1991). The afferent sensory neurones containing SP were found to control vascular permeability in numerous tissues other than the skin, such as the air passages, nasal mucosa, meninges, eyes, urinary bladder and joints (Moskowitz et al, 1979;Bill et al, 1979;Saria et al, 1983;Pernow, 1985;Helme et al, 1985;Lam & Ferrell, 1991).…”

Section: Introductionmentioning

confidence: 99%

A non‐peptide NK₁‐receptor antagonist, RP 67580, inhibits neurogenic inflammation postsynaptically

Moussaoui

Montier

Carruette

et al. 1993

British J Pharmacology

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1 The non-peptide neurokinin NKI-receptor antagonist, RP 67580 (3aR, 7aR), a perhydroisoindolone derivative, powerfully reduced plasma extravasation in rat hind paw skin induced by local application of xylene (ID50 = 0.03 mg kg ', i.v.) or capsaicin (ID50 = 0.06 mg kg-', i.v.), or by i.v. injection of exogenous substance P (SP) or septide ([pGlu6,) (IDm = 0.04-0.05 mg kg ', i.v.). RP 67580 (1 mg kg-', i.v.) also abolished capsaicin-induced nasal fluid hypersecretion (by 82 ± 5%). These effects were found to be stereospecific, the enantiomer, RP 68651 (3aS, 7aS), being inactive at lmgkg-', i.v. 2 In rats neonatally treated with capsaicin (50 mg kg-', s.c.), plasma extravasation induced by SP was significantly increased (by 43 ± 7%). RP 67580 (1 mg kg-', i.v.) completely inhibited the SP-induced plasma extravasation in capsaicin neonatally treated-animals, as it did in control animals. This result suggests that RP 67580 acts at the postsynaptic level for the inhibition of plasma extravasation.3 Opioid receptor agonists, ft-(morphine) and ic-(PD-117302) at 10mgkg-', s.c., in contrast to NKI-receptor antagonists, did not inhibit plasma extravasation induced by exogenous SP. They were, however, partially effective against plasma extravasation induced by electrical nerve stimulation (74 ± 4% and 48 ± 9% inhibition at 10 mg kg', s.c. of morphine and PD-1 17302, respectively, compared to 90 ± 3% inhibition obtained with RP 67580, 3 mg kg-', s.c.). These results indicate the presynaptic action of opioid receptor agonists, in contrast to the postsynaptic action of NK,-receptor antagonists for the inhibition of plasma extravasation. 4 Ligature of the saphenous nerve distal to the point of electrical stimulation, local application of lignocaine to the saphenous nerve, neonatal capsaicin pretreatment, and colchicine at very low doses (120 jig kg' day-' given for 3 days) were found to prevent plasma extravasation elicited by electrical nerve stimulation. 5 The foregoing results demonstrate that the non-peptide NK,-receptor antagonist, RP67580, is a potent inhibitor of plasma extravasation induced in skin by NK,-receptor agonists, by local application of chemical irritants (capsaicin or xylene) or by electrical nerve stimulation. Moreover, opioid receptor agonists and colchicine inhibit plasma extravasation induced by electrical nerve stimulation but not that elicited by exogenous SP. Therefore, it is possible to inhibit neurogenic inflammation either at the presynaptic level with opioid receptor agonists and colchicine, or at the postsynaptic level with NK,-receptor antagonists, and that the new non-peptide NK,-receptor antagonists may have a great potential for alleviation of inflammation in various pathological syndromes in man.

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Section: Introductionmentioning

confidence: 99%

A non‐peptide NK₁‐receptor antagonist, RP 67580, inhibits neurogenic inflammation postsynaptically

Moussaoui

Montier

Carruette

et al. 1993

British J Pharmacology

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“…Peripheral nerves release transmitters and peptides, including CGRP (Lam and Ferrell, 1991;Mulder et al, 1997;Lawand et al, 2000). Unilateral inflammation causes alterations in nociceptive thresholds (Stein et al, 1988), and notably, mice deficient in the ␣-CGRP gene fail to develop secondary hyperalgesia after inflammation (Zhang et al, 2001).…”

Section: Inflammation Increases Sensory Neuropeptides and Painmentioning

confidence: 99%

Activin Induces Tactile Allodynia and Increases Calcitonin Gene-Related Peptide after Peripheral Inflammation

Slambrouck

Berti‐Mattera

et al. 2005

J. Neurosci.

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Calcitonin gene-related peptide (CGRP) is a sensory neuropeptide important in inflammatory pain that conveys pain information centrally and dilates blood vessels peripherally. Previous studies indicate that activin A increases CGRP-immunoreactive (IR) sensory neurons in vitro, and following wound, activin A protein increases in the skin and more neurons have detectable CGRP expression in the innervating dorsal root ganglion (DRG). These data suggest some adult sensory neurons respond to activin A or other target-derived factors with increased neuropeptide expression. This study was undertaken to test whether activin contributes to inflammatory pain and increased CGRP and to learn which neurons retained plasticity. After adjuvant-induced inflammation, activin mRNA, but not NGF or glial cell line-derived neurotrophic factor, increased in the skin. To examine which DRG neurons increased CGRP immunoreactivity, retrograde tracer-labeled cutaneous neurons were characterized after inflammation. The proportion and size of tracer-labeled DRG neurons with detectable CGRP increased after inflammation. One-third of CGRP-IR neurons that appear after inflammation also had isolectin B4 binding, suggesting that some mechanoreceptors became CGRP-IR. In contrast, the increased proportion of CGRP-IR neurons did not appear to come from RT97-IR neurons. To learn whether central projections were altered after inflammation, CGRP immunoreactivity in the protein kinase C␥-IR lamina IIi was quantified and found to increase. Injection of activin A protein alone caused robust tactile allodynia and increased CGRP in the DRG. Together, these data support the hypothesis that inflammation and skin changes involving activin A cause some sensory neurons to increase CGRP expression and pain responses.

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“…Furthermore, they have a trophic role, and they cooperate with the immune system (Ferrell and Lam, 1996). SP releases inflammatory mediators from mast cells and induces the secretion of prostaglandin E 2 and collagenase from synoviocytes and interleukin-1 from macrophages (Lam and Ferrell, 1991). These mechanisms are also implicated in chronic inflammatory reactions, such as rheumatoid arthritis (Jorgensen and Sany, 1994), which is a major problem in medicine.…”

mentioning

confidence: 99%

Role of Transient Receptor Potential Vanilloid 1 Receptors in Adjuvant-Induced Chronic Arthritis: In Vivo Study Using Gene-Deficient Mice

Szabó

Helyes²,

Sándor³

et al. 2005

J Pharmacol Exp Ther

137

123

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The transient receptor potential vanilloid 1 (TRPV1) receptor is a nonselective cation channel localized on a subset of primary sensory neurons and can be activated by a wide range of stimuli. The present study investigated the role of this receptor in chronic arthritis evoked by complete Freund's adjuvant (CFA) using TRPV1 receptor gene-deleted (TRPV1 Ϫ/Ϫ ) mice and wildtype counterparts (TRPV1 ϩ/ϩ ). In TRPV1 ϩ/ϩ mice, CFA injected intraplantarly into the left hindpaw and the root of the tail induced swelling of the injected and contralateral paws up to 130 and 28%, respectively, measured by plethysmometry throughout 18 days. Mechanonociceptive threshold measured with dynamic plantar aesthesiometry was decreased by 50 and 18% on the injected and contralateral paws, respectively. Histological examination and scoring of the tibiotarsal joints revealed marked arthritic changes in wild-type mice. In TRPV1 Ϫ/Ϫ animals edema, histological score and mechanical allodynia were significantly smaller. Daily treatment with the lipoxygenase inhibitor nordihydroguaretic acid (NDGA), the cyclooxygenase inhibitor indomethacin, the bradykinin B2 receptor antagonist

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Specific neurokinin receptors mediate plasma extravasation in the rat knee joint

Cited by 67 publications

References 24 publications

A non‐peptide NK₁‐receptor antagonist, RP 67580, inhibits neurogenic inflammation postsynaptically

A non‐peptide NK₁‐receptor antagonist, RP 67580, inhibits neurogenic inflammation postsynaptically

Activin Induces Tactile Allodynia and Increases Calcitonin Gene-Related Peptide after Peripheral Inflammation

Role of Transient Receptor Potential Vanilloid 1 Receptors in Adjuvant-Induced Chronic Arthritis: In Vivo Study Using Gene-Deficient Mice

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Specific neurokinin receptors mediate plasma extravasation in the rat knee joint

Cited by 67 publications

References 24 publications

A non‐peptide NK1‐receptor antagonist, RP 67580, inhibits neurogenic inflammation postsynaptically

A non‐peptide NK1‐receptor antagonist, RP 67580, inhibits neurogenic inflammation postsynaptically

Activin Induces Tactile Allodynia and Increases Calcitonin Gene-Related Peptide after Peripheral Inflammation

Role of Transient Receptor Potential Vanilloid 1 Receptors in Adjuvant-Induced Chronic Arthritis: In Vivo Study Using Gene-Deficient Mice

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A non‐peptide NK₁‐receptor antagonist, RP 67580, inhibits neurogenic inflammation postsynaptically

A non‐peptide NK₁‐receptor antagonist, RP 67580, inhibits neurogenic inflammation postsynaptically