In order to reveal the role of axon reflexes and sensory receptors in sensory neuropeptide release in response to capsaicin, liberation of substance P, calcitonin gene-related peptide and somatostatin from isolated rat tracheae was investigated in the presence of voltage-sensitive Na+ and Ca2+ channel blocking agents. Neuropeptide release induced by capsaicin (10 nM) remained unchanged in the presence of 25 mM lidocaine, 1 μM tetrodotoxin or the N-type Ca2+ channel inhibitor, ω-conotoxin GVIA (100-300 nM). Peptide release by 100 pulses of 2 Hz field stimulation was prevented by lidocaine or tetrodotoxin. Omega-agatoxin TK (250 nM) significantly inhibited and Cd2+ (200 μM) prevented capsaicin-induced neuropeptide release. These results suggest that chemical stimulation-induced neuropeptide release does not involve activation of fast Na+ channels or N- and P-type voltage-dependent Ca2+ channels, but contribution of Q-type Ca2+ channels is possible. Sensory neuropeptides are released by capsaicin from sensory receptors without axon reflexes.
- CGRP (calcitonin gene-related peptide)
- Neuropeptide release
- Substance P
ASJC Scopus subject areas