Respiratory actions of vanilloid receptor agonists in the nucleus of the solitary tract: comparison of resiniferatoxin with non-pungent agents and anandamide

Geraghty, Dominic P. and Mazzone, Stuart B. (2002) Respiratory actions of vanilloid receptor agonists in the nucleus of the solitary tract: comparison of resiniferatoxin with non-pungent agents and anandamide. British Journal of Pharmacology, 137 6: 919-927. doi:10.1038/sj.bjp.0704931


Author Geraghty, Dominic P.
Mazzone, Stuart B.
Title Respiratory actions of vanilloid receptor agonists in the nucleus of the solitary tract: comparison of resiniferatoxin with non-pungent agents and anandamide
Journal name British Journal of Pharmacology   Check publisher's open access policy
ISSN 0007-1188
1476-5381
Publication date 2002-11
Sub-type Article (original research)
DOI 10.1038/sj.bjp.0704931
Open Access Status Not yet assessed
Volume 137
Issue 6
Start page 919
End page 927
Total pages 9
Place of publication Chichester, West Sussex PO19 8SQ United Kingdom
Publisher John Wiley & Sons
Language eng
Formatted abstract
1. Activation of vanilloid receptors on sensory nerve terminals in the commissural nucleus of the solitary tract (cNTS) of rats with capsaicin, produces respiratory slowing. In this study, we used microinjection techniques employing pungent and non-pungent vanilloids to further characterize vanilloid receptors in the cNTS.

2. Microinjection of the pungent vanilloid, resiniferatoxin (RTX), into the cNTS of urethane-anaesthetized rats, dose-dependently reduced respiratory rate without affecting tidal volume. RTX was 20 fold more potent at slowing respiration (∼ED50, 100 pmol) than capsaicin (∼ED50, 2 nmol). Doses of RTX greater than 100 pmol caused either irregular (dyspnoeic) breathing or terminal apnoea (>250 pmol). The respiratory slowing response to RTX (75 pmol), was dose-dependently attenuated by injecting RTX (but not vehicle) into the same site 60 min earlier.

3. The non-pungent phorbol derivative of RTX, phorbol 12-phenylacetete 13-acetate 20-homovanillate (PPAHV, 0.1-1 nmol), also slowed respiration (ED50, ∼1 nmol) and almost abolished response to RTX (75 pmol) injected into the same site 60 min later.

4. In contrast to RTX, PPAHV and capsaicin, the putative endogenous vanilloid receptor agonist, arachidonyl ethanolamide (AEA), and non-pungent capsaicin derivative, olvanil, had no direct effect on respiration. However, both AEA and olvanil dose-dependently reduced the respiratory response to injection of RTX (75 pmol) 60 min later into the same site (EC50s, for AEA and olvanil, ∼2 and 0.2 nmol, respectively).

5. These studies suggest that both pungent and non-pungent vanilloids interact with vanilloid receptors in the cNTS. However, whereas RTX and PPAHV activate and subsequently desensitize vanilloid receptors on sensory nerve terminals in the cNTS, olvanil and AEA fail to activate despite readily desensitizing responses to RTX in this region.
Keyword C-fibre
Desensitization
Nucleus of the solitary tract
Tachykinins
Vanilloid
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: School of Biomedical Sciences Publications
 
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