The effect of a tachykinin NK<sub>1</sub> receptor antagonist, SR140333, on oedema formation induced in rat skin by venom from the <i>Phoneutria nigriventer</i> spider

Palframan, Roger; Costa, Soraia K.P.; Wilsoncroft, P.; Antunes, Edson; Nucci, Gilberto De; Brain, Susan D.

doi:10.1111/j.1476-5381.1996.tb15402.x

Cited by 42 publications

(18 citation statements)

References 11 publications

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“…Previous studies using the tachykinin NK1R antagonist SR140333 indicate that cutaneous edema can be mediated by NK1Rs and is independent of histamine effects (613). This finding is supported by experiments using NK1R knockout mice, which showed that intradermally injected SP, NK1R agonists (GR-73632), and the mast cell-degranulating agent compound 48/80 induced dosedependent cutaneous edema in wild-type mice that was lacking in knockout mice.…”

Section: Tachykinins and Neurokinin Receptorssupporting

confidence: 75%

Neuronal Control of Skin Function: The Skin as a Neuroimmunoendocrine Organ

Roosterman¹,

Goerge

Schneider

et al. 2006

Physiological Reviews

556

521

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This review focuses on the role of the peripheral nervous system in cutaneous biology and disease. During the last few years, a modern concept of an interactive network between cutaneous nerves, the neuroendocrine axis, and the immune system has been established. We learned that neurocutaneous interactions influence a variety of physiological and pathophysiological functions, including cell growth, immunity, inflammation, pruritus, and wound healing. This interaction is mediated by primary afferent as well as autonomic nerves, which release neuromediators and activate specific receptors on many target cells in the skin. A dense network of sensory nerves releases neuropeptides, thereby modulating inflammation, cell growth, and the immune responses in the skin. Neurotrophic factors, in addition to regulating nerve growth, participate in many properties of skin function. The skin expresses a variety of neurohormone receptors coupled to heterotrimeric G proteins that are tightly involved in skin homeostasis and inflammation. This neurohormone-receptor interaction is modulated by endopeptidases, which are able to terminate neuropeptide-induced inflammatory or immune responses. Neuronal proteinase-activated receptors or transient receptor potential ion channels are recently described receptors that may have been important in regulating neurogenic inflammation, pain, and pruritus. Together, a close multidirectional interaction between neuromediators, high-affinity receptors, and regulatory proteases is critically involved to maintain tissue integrity and regulate inflammatory responses in the skin. A deeper understanding of cutaneous neuroimmunoendocrinology may help to develop new strategies for the treatment of several skin diseases.

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Section: Tachykinins and Neurokinin Receptorssupporting

confidence: 75%

Neuronal Control of Skin Function: The Skin as a Neuroimmunoendocrine Organ

Roosterman¹,

Goerge

Schneider

et al. 2006

Physiological Reviews

556

521

View full text Add to dashboard Cite

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“…Substance P acts though NK 1 receptors, whereas neurokinins A and B act through NK 2 receptors. Tachykinins have been implicated in the edema caused by venoms of the spider P. nigriventer (Palframan et al, 1996;Costa et al, 1997Costa et al, , 2001) and the social wasp Polistes lanio lanio (Yshii et al, 2009), and in itching caused by P. nigriventer venom (Costa et al, 2006). Because these responses are abolished by blockade of NK 1 but not NK 2 receptors, and attenuated in NK 1 knockout mice, the conclusion is that substance P is the main mediator involved.…”

Section: Discussionmentioning

confidence: 94%

“…Although there has been no systematic screening for the presence of histamine in theraphosid venoms, mass spectrometric analysis of venom from Hapopelma lividum indicated only a very low content of histamine (0.14%) in this venom (Moore et al, 2009). In contrast, histamine is involved in P. nigriventer venom-induced edema in rat skin (Palframan et al, 1996) and hind paw (Costa et al, 2000(Costa et al, , 2001 following the activation of mast cells. Histamine has a role in the vascular permeability caused by Atrax spp.…”

Section: Discussionmentioning

confidence: 99%

Pharmacological Characterization of the Edema Caused by Vitalius dubius (Theraphosidae, Mygalomorphae) Spider Venom in Rats

Silva

Linardi

Antunes

et al. 2015

Journal of Pharmacology and Experimental Therapeutics

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Bites by tarantulas (Theraphosidae, Mygalomorphae) in humans can result in mild clinical manifestations such as local pain, erythema, and edema. Vitalius dubius is a medium-sized, nonaggressive theraphosid found in southeastern Brazil. In this work, we investigated the mediators involved in the plasma extravasation caused by V. dubius venom in rats. The venom caused dose-dependent (0.1-100 mg/site) edema in rat dorsal skin. This edema was significantly inhibited by butyl]benzamide) (SR48968, a neurokinin NK 2 receptor antagonist) had no effect on the venom-induced increase in vascular permeability. In rat hind paws, the venom-induced edema was attenuated by ketoprofen (a nonselective COX inhibitor) administered 15 minutes postvenom. Preincubation of venom with commercial antiarachnid antivenom attenuated the venom-induced edema. These results suggest that the enhanced vascular permeability evoked by V. dubius venom involves serotonin, COX products, neurokinin NK 1 receptors, and nitric oxide formation. The attenuation of hind paw edema by ketoprofen suggests that COX inhibitors could be useful in treating the local inflammatory response to bites by these spiders.

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“…It has been shown that the oedematous effect induced by PNV in rats involves the generation of kinins and the stimulation of tackykinin receptors. This effect also depends on the histamine, serotonin and polypeptides contained in the venom [5], [6], [7], [8]. Because pain may occur after PNV envenomation even in the absence of oedema, the mechanisms involved in these responses could be distinct.…”

Section: Introductionmentioning

confidence: 99%

Mechanisms Involved in the Nociception Triggered by the Venom of the Armed Spider Phoneutria nigriventer

et al. 2013

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Background The frequency of accidental spider bites in Brazil is growing, and poisoning due to bites from the spider genus Phoneutria nigriventer is the second most frequent source of such accidents. Intense local pain is the major symptom reported after bites of P. nigriventer, although the mechanisms involved are still poorly understood. Therefore, the aim of this study was to identify the mechanisms involved in nociception triggered by the venom of Phoneutria nigriventer (PNV).Methodology/Principal Findings Twenty microliters of PNV or PBS was injected into the mouse paw (intraplantar, i.pl.). The time spent licking the injected paw was considered indicative of the level of nociception. I.pl. injection of PNV produced spontaneous nociception, which was reduced by arachnid antivenin (ArAv), local anaesthetics, opioids, acetaminophen and dipyrone, but not indomethacin. Boiling or dialysing the venom reduced the nociception induced by the venom. PNV-induced nociception is not dependent on glutamate or histamine receptors or on mast cell degranulation, but it is mediated by the stimulation of sensory fibres that contain serotonin 4 (5-HT4) and vanilloid receptors (TRPV1). We detected a kallikrein-like kinin-generating enzyme activity in tissue treated with PNV, which also contributes to nociception. Inhibition of enzymatic activity or administration of a receptor antagonist for kinin B2 was able to inhibit the nociception induced by PNV. PNV nociception was also reduced by the blockade of tetrodotoxin-sensitive Na+ channels, acid-sensitive ion channels (ASIC) and TRPV1 receptors.Conclusion/SignificanceResults suggest that both low- and high-molecular-weight toxins of PNV produce spontaneous nociception through direct or indirect action of kinin B2, TRPV1, 5-HT4 or ASIC receptors and voltage-dependent sodium channels present in sensory neurons but not in mast cells. Understanding the mechanisms involved in nociception caused by PNV are of interest not only for better treating poisoning by P. nigriventer but also appreciating the diversity of targets triggered by PNV toxins.

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The effect of a tachykinin NK₁ receptor antagonist, SR140333, on oedema formation induced in rat skin by venom from the Phoneutria nigriventer spider

Abstract: 1 The possibility that tachykinin NK, receptors

Cited by 42 publications

References 11 publications

Neuronal Control of Skin Function: The Skin as a Neuroimmunoendocrine Organ

Neuronal Control of Skin Function: The Skin as a Neuroimmunoendocrine Organ

Pharmacological Characterization of the Edema Caused by Vitalius dubius (Theraphosidae, Mygalomorphae) Spider Venom in Rats

Mechanisms Involved in the Nociception Triggered by the Venom of the Armed Spider Phoneutria nigriventer

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The effect of a tachykinin NK1 receptor antagonist, SR140333, on oedema formation induced in rat skin by venom from the Phoneutria nigriventer spider

Abstract: 1 The possibility that tachykinin NK, receptors

Cited by 42 publications

References 11 publications

Neuronal Control of Skin Function: The Skin as a Neuroimmunoendocrine Organ

Neuronal Control of Skin Function: The Skin as a Neuroimmunoendocrine Organ

Pharmacological Characterization of the Edema Caused by Vitalius dubius (Theraphosidae, Mygalomorphae) Spider Venom in Rats

Mechanisms Involved in the Nociception Triggered by the Venom of the Armed Spider Phoneutria nigriventer

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The effect of a tachykinin NK₁ receptor antagonist, SR140333, on oedema formation induced in rat skin by venom from the Phoneutria nigriventer spider