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Sensory neuropeptide effects in human skin
R W Fuller1, T B Conradson, C M Dixon
1Department of Clinical Pharmacology, Royal Postgraduate Medical School, London.
British Journal of Pharmacology
|December 1, 1987
Summary
Sensory neuropeptides like Substance P cause skin flare and wheals through axon reflexes and direct effects. Calcitonin gene-related peptide induces prolonged local redness, with responses modulated by histamine and aspirin.
Area of Science:
- Cutaneous neuropharmacology
- Dermatology
- Neuroimmunology
Background:
- Sensory neuropeptides are implicated in skin reactions following trauma.
- Understanding the specific roles of neuropeptides in cutaneous responses is crucial.
Purpose of the Study:
- To investigate the effects of four sensory neuropeptides on human skin.
- To determine the relative potencies and mechanisms of action of Substance P, Neurokinin A, Neurokinin B, and CGRP in causing flare and wheal responses.
Main Methods:
- Intradermal injections of four sensory neuropeptides (Substance P, NKA, NKB, CGRP) in 28 normal subjects.
- Assessment of flare and wheal formation at and distant from injection sites.
- Evaluation of the effects of H1-histamine antagonist (terfenadine) and aspirin on neuropeptide-induced responses.
Main Results:
- Substance P, NKA, and NKB induced distant flares via axon reflexes, with Substance P being the most potent.
- CGRP caused a dose-dependent local erythema with prolonged duration, but did not consistently induce wheals.
- Terfenadine inhibited histamine and NKA responses, while aspirin inhibited flares from SP, NKA, and CGRP, and NKA-induced wheals.
Conclusions:
- Tachykinins mediate distant flares partly through histamine and cyclo-oxygenase products, but induce wheals directly on the microvasculature.
- The neuropeptide receptor involved in wheal response appears to be SPp or NK1.
- CGRP acts as a direct, prolonged vasodilator.