Peptide release, capsaicin-evoked

Abrahamsson C (2000) Neuropeptide Y1- and Y2-receptor-mediated cardiovascular effects in the anaesthetized guinea pig, rat, and rabbit. J Cardiovasc Pharmacol 36 451-8 Ackley MA, Hurley RW, Virnich DE et al (2001) A cellular mechanism for the antinociceptive effect of a kappa opioid receptor agonist. Pain 91 377-88 Aimone LD, Yaksh TL (1989) Opioid modulation of capsaicin-evoked release of substance P from rat spinal cord in vivo. Peptides 10 1127-31... 

Eflington HC, Cotter MA, Cameron NA, Ross RA (2002) The effect of cannabinoids on capsaicin-evoked caldtonin gene-related peptide (CGRP) release from the isolated paw skin of diabetic and non-diabetic rats. Neuropharmacology 42 966-975 Endres-Becker J, HeppenstaU PA, Mousa SA, Labuz D, Oksche A, Schafer M, Stein C, Zollner C (2007) Mu-opioid receptor activation modulates transient receptor potential vanilloid 1... 

Finally, cannabinoids inhibit the release of neuropeptides like calcitonin gene-related peptide (CGRP), substance P and somatostatin from sensory neurons (Table 4). Capsaicin or electrical stimulation was used to evoke neuropeptide release. In some of these studies, the endocannabinoid anandamide was used, which has a dual effect on neuropeptide release from sensory neurons. Anandamide possesses an inhibitory effect mediated via CBi receptors at low concentrations and... 

The role of peptidergic neurons is not so clear. Capsaicin, the hot chile pepper chemical that evokes release of peptide transmitters from several types of sensory nerves, has been shown to reproduce some of the signs of bronchial hyperreactivity in animal and human experiments. These findings led to the proposal that sensitization of afferent nerve endings played a major role in chronic airway hyperreactivity. However, peptide transmitter antagonists have not been able to prevent bronchoconstriction in several models. Clearly, much remains to be learned about airway pharmacology. 

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