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Toxin Tx2‐6 from the spider “Phoneutria nigriventer” improves the impaired erectile function in DOCA‐Salt hypertensive rats
Author(s) -
Nunes Kenia P.,
Gonçalves Andrey C. C.,
Lanza Luciana F.,
Cortes Steyner f.,
Nascimento Marta C.,
Richardson Michael,
Pimenta Adriano M. C.,
Webb R. Clinton,
de Lima Maria Elena,
Leite Romulo
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a881-c
Subject(s) - stimulation , erectile dysfunction , medicine , erectile function , pharmacology , nitric oxide , endocrinology , chemistry , anesthesia
Accidents involving the venom of spider P. nigriventer are characterized by different symptoms including priapism. The aim of this study is to investigate the role of the toxin Tx2‐6, a peptide extracted from the venom of P. nigriventer, in the penile erection. Erectile function was measured in urethane anesthetized Wistar rats (230–250g) by continuous monitoring mean arterial pressure (MAP) and intracavernosal pressure (ICP) during electrical stimulation of the major pelvic ganglion. Voltage‐response curves (0.5–3.0V, 12Hz, 0.1ms, 30s each step) were performed before and (15 min) after subcutaneous injection of Tx2‐6 (12 μg/Kg). The erectile response induced by ganglionic stimulation was significantly potentiated after injection of Tx2‐6. Incubation with Tx2‐6 (0,1 and 0,01μg/mL) caused a significant release of NO from rat isolated strips of corpus cavernosum, detected through a NO indicator (DAF‐FM) using confocal microscopy. Subcutaneous injection of Tx2‐6 significantly improved the impaired erectile response induced by ganglionic stimulation in DOCA‐salt hypertensive compared to sham‐operated rats. The results in this study indicate that Tx2‐6 is probably the component of the venom responsible for the priapism observed in poisoning accidents with the P. nigriventer spider, and that Tx2‐6 induces and or potentiates penile erection by facilitating the nitric oxide‐cyclic GMP pathway. Furthermore, our results suggest that Tx2‐6 is a pharmacological tool with a great potential to treat erectile dysfunction. Financial support: CNPq, CAPES, NIH (HL‐74167)