Answers are grounded in this paper and cite their sources.
CGRP is released from capsaicin-sensitive sensory neurons in a Ca(2+)-dependent manner in a variety of peripheral organs as well as from central terminals. The mechanisms for CGRP release by low concentrations of capsaicin, electrical antidromic nerve stimulation, and bradykinin have several similar characteristics regarding sensitivity to TTX, CTX, and alpha 2-adrenoceptor activation. High capsaicin concentration and nicotine evoke CGRP release via other mechanisms. The effects of capsaicin, resiniferatoxin, and SO2 are blocked by RR, which probably inhibits ion fluxes associated with capsaicin receptor activation. CGRP released upon irritation of peripheral branches of primary afferents may evoke a variety of cardiovascular actions and influence motility in the gastrointestinal and urogenital tracts.
No takes yet. Share an insight, caveat, or question.
Lundberg et al. (1992) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: