Citation

Costa SK, De Nucci G, Antunes E, Brain SD. Eur. J. Pharmacol. 1997; 339(2-3): 223-226.

Affiliation

Department of Pharmacology, Faculty of Medical Sciences, UNICAMP, Campinas (SP), Brazil.

Copyright

(Copyright © 1997, Elsevier Publishing)

DOI

unavailable

PMID

9473139

Abstract

Phoneeutria nigriventer venom induces oedema formation when injected in the rat dorsal skin and such oedema is, in part, dependent on the stimulation of tachykinin NK1 receptors. This study investigated whether Phoneutria nigriventer venom acts directly on tachykinin NK1 receptors, or indirectly to activate sensory neurones which in turn release a tachykinin NK1 receptor agonist. The plasma extravasation induced by Phoneutria nigriventer venom (1-10 microg/site) in neonatally capsaicin (8-methyl N-vanillyl-6-nonenamide)-pretreated rats was substantially attenuated (P < 0.05) but the response to either the tachykinin NK1 receptor agonist GR73632 ((deltaAva[L-Pro9, N-MeLeu10] substance P-(7-11) 30 pmol/site) or bradykinin (0.3-3 nmol/site) was not affected. These results indicate that Phoneutria nigriventer venom stimulates sensory nerves indirectly. The lack of effect of capsaicin-pretreatment on the GR73632 and bradykinin responses indicated that the tachykinin NK1 and bradykinin B2 receptors remained functional. There was no evidence to suggest that Phoneutria nigriventer venom contains a tachykinin NK1 receptor agonist.

Language: en