Abstract
Stonustoxin (SNTX) is a 148 kDa, dimeric, hypotensive and lethal protein factor isolated from the venom of the stonefish
Synanceja horrida. SNTX (10–320 ng/ml) progressively causes relaxation of endothelium-intact, phenylephrine (PE)-precontracted rat thoracic aortic rings. The SNTX-induced vasorelaxation was inhibited by
l-
N
G-nitro arginine methyl ester (
l-NAME), suggesting that nitric oxide (NO) contributes to the SNTX-induced response. Interestingly,
d,
l-proparglyglycine (PAG) and β-cyano-
l-alanine (BCA), irreversible and competitive inhibitors of cystathionine-γ-lyase (CSE) respectively, also inhibited SNTX-induced vasorelaxation, indicating that H
2S may also play a part in the effect of SNTX. The combined use of
l-NAME with PAG or BCA showed that H
2S and NO act synergistically in effecting SNTX-induced vasorelaxation.