Capsaicin evokes secretion of nasal fluid and depletes substance P and calcitonin gene‐related peptide from the nasal mucosa in the rat

Abstract

The secretion of nasal fluid was studied in anaesthetized rats after topical application of capsaicin, and of calcitonin gene-related peptide (CGRP) alone or CGRP in combination with substance P (SP). The flow of nasal fluid was stimulated and the secretions collected by a filter paper technique. The concentrations of SP and CGRP in nasal biopsies were determined after topical or systemic administration of capsaicin. 2 Capsaicin (single dose administration) stimulated nasal secretion in a dose-dependent manner. The effect was inhibited by hexamethonium, lignocaine, or by the tachykinin antagonist (D-Pro2, DTrp7' 9)-SP, but not by atropine, or by a combination of the histamine H -receptor antagonist chlorpheniramine and the H2-receptor antagonist ranitidine. 3 When applied cumulatively, capsaicin rapidly produced desensitization. The concentrations of SP and CGRP in the nasal mucosa were reduced by capsaicin 6 days after topical or s.c. administration but not 15 min after topical application of desensitizing doses. 4 CGRP did not stimulate the secretion of nasal fluid and did not alter SP-evoked nasal secretion. 5 The inhibition by hexamethonium of the capsaicin-evoked nasal secretion suggests the involvement of ganglionic reflexes. In addition, the inhibition of the response to capsaicin by (D-Pro2,DTrp7' 9)-SP and lidocaine and the depletion of SP and CGRP after capsaicin indicate the involvement of tachykinin-mediated axon reflexes.

Calcitonin gene-related peptide differentially regulates gene and protein expression in trigeminal glia cells: Findings from array analysis

“…The dissimilarity in the response to CGRP is most likely due to the difference in CGRP concentrations since the method used to establish the glia-enriched cultures was the same in both studies. While the total level of CGRP in trigeminal ganglia is not known, current literature suggests that CGRP content in tissues and exudates can be detected from low nanomolar to micromolar concentrations in normal or pathological conditions, respectively [1,23]. In our studies, it appears that the duration and magnitude of the stimulatory effects of CGRP on cytokine release from trigeminal glia is concentration dependent.…”

TRPA1 is a major oxidant sensor in murine airway sensory neurons

“…In addition, influx of Ca 2+ through TRPA1 may promote the release of proinflammatory peptides from nasal nerve endings. Sensory neuropeptides such as calcitonin gene-related peptide or substance P are known to induce dilation of blood vessels in the nasal mucosa and promote glandular secretion, contributing to irritant-induced nasal obstruction (71,72).…”

Breathtaking TRP Channels: TRPA1 and TRPV1 in Airway Chemosensation and Reflex Control

“…Sensory-autonomic parasympathetic efferent reflex pathways induce secretions from nasal, lacrimatory and salivary glands, and the dilation of vessels in the nasal mucosa and sinuses. Neuropeptides such as Substance P and CGRP, released from chemically stimulated nerve endings, promote neurogenic inflammatory vasodilation and leakage, contributing to narrowing or obstruction of the nasal passages (11, 102). Chemical stimulation of vagal sensory fibers terminating in the glottis and larynx trigger the cough reflex that, similar to sneezing, promotes the extrusion of air, particulates and mucus from the airways.…”