Topical capsaicin pretreatment inhibits axon reflex vasodilatation caused by somatostatin and vasoactive intestinal polypeptide in human skin

Anand, Praveen; Bloom, Stephen R.; McGregor, G.P.

doi:10.1111/j.1476-5381.1983.tb09418.x

Cited by 80 publications

(41 citation statements)

References 28 publications

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“…There is now consistent evidence that release of a neurotransmitter from sensory nerves can be responsible for wheal and distant flare formation following trauma (Jancso et al, 1968;Lembeck & Holzer, 1979;Gazelius & Olgart, 1980;Anand et al, 1983;Lundberg et al, 1983;Kenins et al, 1984). This study suggests wheal formation following trauma may be due to release ofa tachykinin, either SP, NKA or NKB rather than release of CGRP which does not lead to wheal formation.…”

Section: Discussionmentioning

confidence: 59%

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Sensory neuropeptide effects in human skin

Fuller

Conradson

Dixon

et al. 1987

British J Pharmacology

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1Neuropeptides released from sensory nerves may account for cutaneous flare and wheal following local trauma. In 28 normal subjects we have studied the effects of four sensory neuropeptides given by intradermal injection on the forearm or back. 2 All peptides caused a flare distant from the site of injection, presumably due to an axon reflex. Substance P (SP) was the most potent (geometric mean dose causing 50% ofmaximum flare, 4.2 pmol). Neurokinin A (NKA) was the next most potent with neurokinin B (NKB) and calcitonin gene-related peptide (CGRP) the least. The distant flare response to SP, NKA and NKB was maximal at 5 min and disappeared within 2 h. 3 CGRP caused a local erythema over the site of injection at doses above 0.5 pmol which at higher doses lasted for up to 12 h. 4 SP, NKA and NKB caused wheals at doses above 5 pmol with SP and NKB being the most potent. CGRP (up to 250 pmol) did not consistently cause wheal formation. There was no significant effect of coinjection ofCGRP upon the response to SP although there was a tendency for an enhancement ofthe wheal response. 5 The H,-histamine antagonist terfenadine (60mg orally) significantly inhibited the wheal and distant flare response to histamine (5 nmol) and NKA, but not that caused by NKB. The distant flare of CGRP was also reduced but the local erythema was unaltered. 6 Aspirin (600 mg orally) significantly inhibited the distant flare response to SP, NKA and CGRP, but not that caused by NKB or histamine; the local erythema induced by CGRP was unaffected by aspirin. Aspirin also inhibited the wheal formed by NKA but not the wheal induced by the other substances. 7 These results suggest that tachykinins cause a distant flare response partially via the release of histamine and cyclo-oxygenase products, but cause a wheal by a direct effect on the skin microvasculature. The order of potency SP > NKB > NKA suggests that an SPp or NK, receptor is involved in the wheal response. CGRP by contrast has a direct vasodilator effect which is very prolonged.

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Section: Discussionmentioning

confidence: 59%

“…The widespread flare and part of the wheal response are dependent on intact sensory nerves (Jancso et al, 1968) and probably release of sensory neurotransmitters by an axon reflex (Chahl, 1979;Lembeck & Holzer, 1979;Gazelius & Olgart, 1980;Brodin et al, 1981;Anand et al, 1983; 'Author for correspondence.…”

Section: Introductionmentioning

confidence: 99%

Sensory neuropeptide effects in human skin

Fuller

Conradson

Dixon

et al. 1987

British J Pharmacology

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“…Heat could, dependent on the severity of injury, also cause the local release of substances such as histamine, bradykinin or 5-HT which subsequently stimulate SP fibres (Jancs6 et al, 1980). Since peripheral branches of sensory SP neurones may be involved in neurogenic inflammation of the skin in man (Anand et al, 1983), it will be of interest to determine whether inhibition of SP receptors or blockade of SP release could be useful as initial treatment of oedema caused by thermal injury in man.…”

Section: Discussionmentioning

confidence: 99%

Substance P in sensory nerve fibres contributes to the development of oedema in the rat hind paw after thermal injury

Saria¹

1984

British J Pharmacology

114

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1 Immersion of the hind paws of anaesthetized rats in hot water for 5 min induced massive plasma protein leakage as indicated by extravasation of Evans blue dye in the skin. The threshold temperature which caused noticeable plasma extravasation was 45°C, a maximal response was obtained between 55°C and 60°C. 2 Pretreatment of rats 2 days after birth with 50mg kg-capsaicin significantly reduced the Evans blue extravasation induced by hot water at 50°C, 55°C and 60°C, whereas guanethidine pretreatment 24 h before the experiment caused a significantly increased response at 40°C, 45°C and 50°C. 3 When Evans blue was injected between 10 and 120 min after immersion of the paw in hot water, a significant extravasation of the dye was no longer detectable. However, the weight of the paw as well as the weight of the piece of skin taken for Evans blue quantification increased during this period indicating the progressive development of oedema in the skin and underlying tissues. 4 In rats treated with capsaicin as neonates, the increase in paw weight after immersion in water of 50°C for 5 min was significantly delayed during the first hour, but there was no difference after two hours.5 In rats pretreated with D-Argt,D-Pro2,D-Trp7'9, Leull-substance P, a substance P (SP) antagonist, the Evans blue extravasation was significantly reduced. However, the response, which remained in rats treated with capsaicin as neonates was not blocked by the SP-antagonist. 6 It is concluded that activation of peripheral branches of sensory SP neurones contributes to the initial massive protein extravasation and to the subsequent rate of development of oedema following heat injury. Release of histamine did not significantly contribute to this response at the lower temperatures, although the response was reduced by histamine receptor blocking drugs at 55°C and 60°C. Decreasing the sympathetic vasoconstrictor tone by guanethidine resulted in an increased response.

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“…Octreotide and lanreotide (also known as angiopeptin) have both been shown to reduce postprandial splanchnic hyperemia by inducing vasoconstriction in the vessels of the splanchnic bed in humans (Mottet et al 1998). In contrast, somatostatin is an inflammatory (axon reflex) vasodilator in human skin (Anand et al 1983;Wallengren 1997), and it is reasonable to presume that octreotide and similar analogs have the same effect. A phosphodiesterase (PDE) inhibitor with vasodilatory properties caused ''vascular thickening'' consisting of smooth muscle hypertrophy and hyperplasia of the media of arteries and veins secondary to necrotizing arteritis in several anatomic locations in rats after one month of compound administration (Westwood et al 1990).…”

Section: Effect Of Anatomic Location Of Vesselsmentioning

confidence: 99%

Intimal Hyperplasia in Rats after Subcutaneous Injection of a Somatostatin Analog

Wells¹,

Voute²,

Lonchampt

et al. 2009

Toxicol Pathol

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The somatostatin analog octreotide was administered to male and female Sprague-Dawley rats by subcutaneous injection for thirteen weeks at 0 (saline control), 0 (placebo control [mannitol and lactic acid; pH 4.2]), 1.25 mg/kg/day and 2.5 mg/kg/day to explore its potential effect on cutaneous vascular morphology. The placebo caused an increase in the incidence of intimal hyperplasia compared to saline controls in female rats; octreotide increased the incidence and severity of intimal hyperplasia in males and females. Intimal hyperplasia consisted of increased numbers of cells located between the endothelial cell layer and the internal elastic lamina. Severity was based on the degree of compromise of the vascular lumen (regardless of vessel size and number), with severely affected vessels having no visible lumen. Intimal hyperplasia in rats treated with octreotide was considered to be an unexpected and adverse finding, given that this compound and other somatostatin analogs have been investigated as reducers of intimal proliferation or restenosis after angioplasty in humans and that no such lesion has been reported in the literature for this class of compound to date. The induction of intimal hyperplasia by the placebo is also a notable finding; this may be because of the low pH of the formulation.

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Topical capsaicin pretreatment inhibits axon reflex vasodilatation caused by somatostatin and vasoactive intestinal polypeptide in human skin

Cited by 80 publications

References 28 publications

Sensory neuropeptide effects in human skin

Sensory neuropeptide effects in human skin

Substance P in sensory nerve fibres contributes to the development of oedema in the rat hind paw after thermal injury

Intimal Hyperplasia in Rats after Subcutaneous Injection of a Somatostatin Analog

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