Sensory neuropeptide effects in human skin

Fuller, R W; Conradson, T-B; Dixon, Caroline; Crossman, DC; Barnes, Peter J.

doi:10.1111/j.1476-5381.1987.tb11381.x

Cited by 93 publications

(71 citation statements)

References 31 publications

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“…The hypothesis, however, is not consistent with the lack of potentiation in human skin, in which SP is active (Fuller et al, 1987). The potentiation in rat skin has been suggested as being due to vasodilatation (Gamse & Saria, 1985).…”

Section: Drugs and Chemicalscontrasting

confidence: 40%

See 1 more Smart Citation

Effects and interactions of sensory neuropeptides on airway microvascular leakage in guinea‐pigs

Rogers

Belvisi

Aursudkij

et al. 1988

British J Pharmacology

123

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1 We have studied the effect of the sensory neuropeptides substance P (SP), neurokinin A (NKA), neurokinin B (NKB) and calcitonin gene-related peptide (CGRP) on microvascular permeability in guinea-pig airways in vivo and investigated whether CGRP would potentiate the effect of SP. We used the extravasation of intravenously-injected Evans blue dye as an index of permeability. 2 The tachykinins SP, NKA and NKB (0.025-5.Onmol kg-, i.v.) significantly (P <0.05) increased extravasation of dye in a dose-related manner and with a similar pattern of distribution; they were most potent in the trachea and main bronchi, less potent in the larynx and intrapulmonary airways, and had little significant effect in the bladder.3 SP was significantly more potent in causing extravasation of dye than NKA or NKB with ED50 values (nmol kg-1) in the range 0.04-0.1, depending on the airway level, compared with values in the range 0.3-0.7 for the neurokinins. 4 CGRP (0.0025-2.5 nmol kg-1, i.v.) had no significant effect on microvascular permeability and did not potentiate SP-induced extravasation of dye. 5 Each neuropeptide decreased mean arterial blood pressure, indicating vasodilatation, in a doserelated manner. Co-injection of CGRP and SP produced additive decreases in arterial pressure. 6 We conclude that, in guinea-pig airways, tachykinins increase microvascular permeability via tachykinin receptors of the NK-1 sub-type (indicated by an order of potency of SP > NKA = NKB) on endothelial cells. The response appears to be related to mechanisms in addition to vasodilatation. The relevance of the responses to the tachykinins in asthma is discussed. IntroductionElectrical stimulation of the cervical vagus nerves in rat and guinea-pig induces a number of physiological responses including vasodilatation and increased permeability of the microvasculature of the trachea to macromolecules (Lundberg & Saria, 1982;Lundberg et al., 1983). Both responses are preserved in the presence of atropine, hexamethonium or antihistaminic drugs, but are absent in animals pretreated with capsaicin. Capsaicin is the major pungent principle of hot peppers of the plant genus Capsicum and has been shown to deplete primary afferent C-fibres of stored neuropeptides (Buck & Burks, 1986). Capsaicin itself causes a depolarization of afferent Cfibres which induces local effects including vasodilatation and plasma extravasation in guinea-' Author for correspondence.pigs (Lundberg et al., 1984a). The physiological responses may, therefore, be due to release of neuropeptides localized to capsaicin-sensitive nerves. For example, the tachykinin substance P (SP) has been localized to sensory nerves in the airways of several species, including man (Lundberg et al., 1984b). SP and two newer members of the tachykinin family, neurokinin A (NKA) and neurokinin B (NKB) have been shown to increase vascular permeability in guinea-pig trachea (Lundberg et al., 1985) although, of the two neurokinins, only NKA has been localized to capsaisin-sensitive nerves in the guinea-pig (Hua...

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Section: Drugs and Chemicalscontrasting

confidence: 40%

“…Previous studies have demonstrated species differences in regard to potentiation by CGRP of SP-induced microvascular leakage when both are injected intradermally. In rabbit and man (Fuller et al, 1987), CGRP does not potentiate SP-induced wheal. In contrast, there is potentiation in rat skin Gamse & Saria, 1985).…”

Section: Drugs and Chemicalsmentioning

confidence: 99%

Effects and interactions of sensory neuropeptides on airway microvascular leakage in guinea‐pigs

Rogers

Belvisi

Aursudkij

et al. 1988

British J Pharmacology

123

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“…Both neurokinin A (substance K) and neurokinin B (neuromedin K) were extracted from mammalian spinal cord (Kimura et al, 1983;Kangawa et al, 1983;Minamino et al, 1984). Like substance P, neurokinin A and neurokinin B increase microvascular permeability causing local oedema formation when injected into rat skin (Gamse & Saria, 1985) and human skin (Devillier et al, 1986;Fuller et al, 1987). The tachykinins do not possess a common N-terminus (see Table 1) and the neurokinins are >50 times less potent than substance P in stimulating histamine release from rat peritoneal mast cells (Devillier et al, 1986).…”

Section: Introductionmentioning

confidence: 99%

Interactions between the tachykinins and calcitonin gene‐related peptide lead to the modulation of oedema formation and blood flow in rat skin

Brain

Williams

1989

British J Pharmacology

144

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6LY1 The mechanisms involved in tachykinin-induced oedema were investigated in rat skin and interactions between the tachykinins and calcitonin gene-related peptide (CGRP) were studied. 2 Intradermal injections of the tachykinins, substance P, neurokinin A and neurokinin B, stimulated local oedema formation which was in each case potentiated by co-injection of the vasodilator CGRP. Oedema induced by substance P. in the presence and absence of CGRP, was significantly inhibited by pretreatment of rats with a combination of the histamine H1 antagonist, mepyramine, and the 5-hydroxytryptamine antagonist, methysergide. Oedema induced by neurokinin A or B was not inhibited by this pretreatment. 3 Intradermally-injected CGRP induced a long lasting increase in local blood flow, which was measured with a laser Doppler blood flow meter. The simultaneous injection of substance P, but not of the structurally-related neurokinins, caused a loss of the prolonged vasodilator activity of CGRP. 4 These results show that oedema induced by substance P is partially dependent on mast cell amines and that only substance P causes a loss of the prolonged vasodilator activity of CGRP. 5We suggest that the ability of substance P to prevent the persistent vasodilator activity of CGRP may be a direct consequence of substance P-induced activation of mast cells.

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“…The inflammation is inhibited by pretreatment with capsaicin [4,5], which depletes sensory neurons of SP [7], and by SP antagonists [8]. SP and neuro kinin A also increase the vascular permeability in the skin when administered intradermally [9][10][11][12][13]. In addi tion, it has been shown that the reactivity to a variety of stimuli is increased in various tissues and cells of asthmatics [14][15][16][17], Therefore, for better understand ing of the pathophysiology of asthma, it seems to be important to know whether the reactivity to tachykin ins is altered in asthmatics in comparison with that of normal subjects.…”

Section: Introductionmentioning

confidence: 99%

Skin Reactivity to Substance P, Not to Neurokinin A, Is Increased in Allergic Asthmatics

Iwamoto

Kimura²,

Tanaka³

et al. 1990

Int Arch Allergy Immunol

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The tachykinins substance P (SP) and neurokinin A are believed to be major mediators of neurogenic inflammation. To determine whether the skin reactivity to tachykinins is increased in asthmatics, we examined the erythemas and wheals induced by intradermal injections of SP, the C-terminal peptide SP_6–11, the N-terminal peptide SP_1–9 and neurokinin A (10^––⁷––10^––5M) in 10 allergic asthmatics and 9 normal subjects. SP and SP_1–9 induced both erythemas and wheals in a concentration-dependent manner in allergic asthmatics and in normal subjects, whereas SP_6–11 and neurokinin A induced only wheals in both groups. SP induced greater erythemas and wheals in allergic asthmatics than in normal subjects. However, the wheals induced by neurokinin A were not significantly different between the two groups. SP_1–9 also induced greater erythemas and wheals in allergic asthmatics than in normal subjects, whereas the wheals induced by SP_6–11 were not significantly different between the two groups. Therefore, the increased skin reactivity to SP was dependent on the N-terminal peptide but not on the C-terminal peptide. We conclude that the skin reactivity to SP but not to neurokinin A is increased in allergic asthmatics.

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Sensory neuropeptide effects in human skin

Cited by 93 publications

References 31 publications

Effects and interactions of sensory neuropeptides on airway microvascular leakage in guinea‐pigs

Effects and interactions of sensory neuropeptides on airway microvascular leakage in guinea‐pigs

Interactions between the tachykinins and calcitonin gene‐related peptide lead to the modulation of oedema formation and blood flow in rat skin

Skin Reactivity to Substance P, Not to Neurokinin A, Is Increased in Allergic Asthmatics

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