Release of histamine by substance P

Erjavec, F.; Lembeck, Fred; Florjanc-Irman, Tatjana; Skofitsch, Gerhard; Donnerer, Josef; Saria, Alois; Holzer, Peter

doi:10.1007/bf00506259

Cited by 166 publications

(49 citation statements)

References 26 publications

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“…We have previously suggested that SP is an important mediator in capsaicininduced mouse ear edema, since SP antagonists such as spantide and [D-Pro2,D-Trp7,9]-SP inhibit the edema, whereas CGRP8_37, a CGRP antagonist, has little effect (3). SP is considered to induce the inflammatory response by increasing vascular permeability through the release of vasoactive amines from mast cells (35,36) and activation of NK1 receptors (33,37). Therefore, a histamine H1 blocker and tachykinin antagonists are expected to have inhibitory effects on neurogenic inflammation (38,39).…”

Section: Discussionmentioning

confidence: 99%

Participation of Serotonin in Capsaicin-Induced Mouse Ear Edema

Inoue

Nagata

Kinoshita

1995

Japanese Journal of Pharmacology

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ABSTRACT-We investigated the involvement of serotonin (5-HT) in mouse ear edema induced by topical application of capsaicin (250 ,ug/ear). Application of capsaicin to the ear caused degranulation of mast cells in skin connective tissue. Capsaicin-induced ear edema was significantly inhibited by preadministration of 5-HT2 receptor antagonists such as ketanserin (2 mg/kg, i.v.) and LY 53857 (1 mg/kg, i.v.), but not 5-HT1-, 5-HT3-and 5-HT4-receptor antagonists. Intradermal injection of a-methyl 5-HT (5-HT2-receptor agonist) and 5-HT into ear skin produced edema formation more potently than 8-OH-DPAT (5-HT1A agonist) and 2-methyl 5-HT (5-HT3 agonist). 5-HT2 antagonists markedly suppressed the edema response to 5-HT and its receptor agonists, whereas any antagonist for 5-HT1, 5-HT3 and 5-HT4-receptors had no effect. Furthermore, 5-HT2-receptor antagonists partly prevented ear edema in response to substance P (SP), a putative mediator of capsaicin-induced edema, and compound 48/80, a releaser of vasoactive amines from mast cells. These results suggest that 5-HT released from mast cells is partly involved in the development of capsaicin-induced mouse ear edema via 5-HT2 receptors in the ear skin.Keywords: Capsaicin, Serotonin (5-HT), Ear edema (mouse), 5-HT receptor, 5-HT-receptor antagonist Capsaicin (8-methyl-N-vanillyl-6-nonenamide), the pungent substance contained in many red peppers, evokes neurogenic inflammatory responses such as axon reflex vasodilation, plasma extravasation and painful sensitization (1). Topical application of capsaicin to the mouse ear produces neurogenic skin inflammation (2, 3), which may be mediated by neuropeptides including substance P (SP) released through activation of primary afferent sensory neurons. Virus and Gebhart (4) have suggested that in addition to SP, serotonin (5-HT) also plays a role in the pharmacological activity of capsaicin. Others have reported that treatment of newborn rats with capsaicin causes an increase in the concentrations of histamine and 5-HT in the rat skin as a result of changes of the mast cell system in response to the permanent degeneration of sensory nerves (5). In fact, evidence exists to indicate that peripheral nerve endings and mast cells are in close spatial and functional association (6 -8). Previous studies have found that methysergide is effective in inhibiting capsaicin-induced mouse ear edema (3). However, clear evidence for the involvement of 5-HT in capsaicin-induced inflammation is lacking.5-HT receptors have been classified into at least four subtypes: 5-HT1, 5-HT2, 5-HT3 and 5-HT4 (9, 10). Among them, 5-HT2 receptors participate in the increase of cutaneous vascular permeability induced by 5-HT in rats (11, 12). 5-HT3 receptors are located on neurons and elicit depolization which results in transmitter release from parasympathetic, sympathetic, sensory and enteric neurons (13). Recent studies have shown that neuropeptides are partly released by mediation of 5-HT3 receptor from capsaicin-sensitive afferent neurons (14). These evidence sugg...

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Section: Discussionmentioning

confidence: 99%

Participation of Serotonin in Capsaicin-Induced Mouse Ear Edema

Inoue

Nagata

Kinoshita

1995

Japanese Journal of Pharmacology

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“…From these studies it has been shown that noradrenaline reduces the release of histamine from mast cells caused by antigens, dextran, acetylcholine or by the compound 48/80 (1,12). Acetylcholine, on the contrary, induces the release of histamine from mast cells (13) as do various neuropeptides (11,19,31).…”

mentioning

confidence: 99%

Suggestive evidence for a functional association between mast cells and symphathetic nerves in meningeal membranes.

Ferrante

Rícci

Felici

et al. 1990

Acta Histochem. Cytochem

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“…Reversibly, SP and CGRP probably stimulate histamine release from mast cells and potentiates histamine action (Erjavec et al, 1981;Piotrowski & Foreman, 1986;Lowman et al, 1988;Ottosson & Edvinsson, 1997). Con®rming this observation, Takeda and Imamura demonstrated that capsaicin-induced histamine release in the guinea-pig is prevented by prior destruction of sensory C-®bres by systemic capsaicin pretreatment (Takeda et al, 1993;Imamura et al, 1996).…”

Section: Discussionmentioning

confidence: 95%

Influence of TASP‐V, a novel neuropeptide Y (NPY) Y₂ agonist, on nasal and bronchial responses evoked by histamine in anaesthetized pigs and in humans

Malis¹,

Grouzmann²,

Morel³

et al. 1999

British J Pharmacology

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1 In nine anaesthetized pigs we have studied the in¯uence of intranasal or intrabronchial pretreatment with TASP-V, a neuropeptide Y (NPY) Y 2 agonist formed by the attachment of NPY 21-36 to a template-assembled synthetic peptide (TASP), on the functional responses to subsequent intranasal or intrabronchial histamine challenge. 2 In a parallel study, subjective and objective nasal airway resistance (NAR) increase following intranasal histamine challenge was evaluated in 11 healthy volunteers after TASP-V or placebo pretreatment. 3 In pigs, increase in sphenopalatine blood¯ow induced by histamine dihydrochloride nasal spray (0.25 mg kg 71 in 3 ml of saline) was signi®cantly reduced by 65% (P50.05) following intranasal pretreatment with 10 mg kg 71 of TASP-V. Bronchoconstriction induced by histamine dihydrochloride nebulization (0.5 mg kg 71 in 3 ml of saline) was signi®cantly attenuated by 25 and 55% following aerosolized pretreatment with TASP-V analogue at 10 and 20 mg kg 71 , respectively. 4 In healthy volunteers, objective increase in NAR and reduction in nasal minimal cross section area (MCSA) induced by intranasal spray of histamine dihydrochloride (15 mg kg 71 in 200 ml of saline) were signi®cantly attenuated by 50% following local pretreatment with 1.275 mg kg 71 of TASP-V when compared with saline. 5 It is concluded that intranasal or intrabronchial pretreatment with TASP-V reduced nasal obstruction and bronchoconstriction evoked by histamine challenge in the pig. In healthy human volunteers, this agent attenuated NAR increase and MCSA reduction induced by intranasal application of histamine.

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Release of histamine by substance P

Cited by 166 publications

References 26 publications

Participation of Serotonin in Capsaicin-Induced Mouse Ear Edema

Participation of Serotonin in Capsaicin-Induced Mouse Ear Edema

Suggestive evidence for a functional association between mast cells and symphathetic nerves in meningeal membranes.

Influence of TASP‐V, a novel neuropeptide Y (NPY) Y₂ agonist, on nasal and bronchial responses evoked by histamine in anaesthetized pigs and in humans

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Release of histamine by substance P

Cited by 166 publications

References 26 publications

Participation of Serotonin in Capsaicin-Induced Mouse Ear Edema

Participation of Serotonin in Capsaicin-Induced Mouse Ear Edema

Suggestive evidence for a functional association between mast cells and symphathetic nerves in meningeal membranes.

Influence of TASP‐V, a novel neuropeptide Y (NPY) Y2 agonist, on nasal and bronchial responses evoked by histamine in anaesthetized pigs and in humans

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Product

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Influence of TASP‐V, a novel neuropeptide Y (NPY) Y₂ agonist, on nasal and bronchial responses evoked by histamine in anaesthetized pigs and in humans