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 NK 1 receptors. This study investigated whether Phoneutria nigriventer venom acts directly on tachykinin NK 1 receptors, or indirectly to activate sensory neurones which in turn release a tachykinin NK 1 receptor agonist. The plasma extravasation induced by Phoneutria nigriventer venom (1–10 μg/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 NK 1 receptor agonist GR73632 (( δAva[ l-Pro 9, 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 NK 1 and bradykinin B 2 receptors remained functional. There was no evidence to suggest that Phoneutria nigriventer venom contains a tachykinin NK 1 receptor agonist.
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