The effects of the sodium channel activators veratridine and batrachotoxin on isolated rat aorta were investigated. Veratridine caused gradual contraction, independent of the presence of endolhelium, with an EC50 of 35 μM. Batrachotoxin (1 μM) also induced contraction. Both effects were completely inhibited by the sodium channel blocker tetrodotoxin (1 μM). The veratridine (60 μM)-induced contraction was inhibited by nifedipine (0.1 μM). In the absence of extracellular Ca2+, veratridine (60 μm) did not cause contraction. Sodium nitroprusside (80 nM), acetylcholine (10 μM) and isoproterenol (1 μM) caused relaxation of rings precontracted with veratridine (60 μM). An inhibitor of endothelium-derived relaxing factor (EDRF) synthase, Nω-nitro-L-arginine methyl ester (L-NAME) (0.65 mM). enhanced the veratridine-induced contraction in rings with an intact endothelium, which suggests that EDRF was being released during the veratridine-induced contraction. These results show that the activation of sodium channels on smooth muscle cells induces a contraction that is probably mediated by Ca2+ influx through voltage-dependent Ca2+ channels.
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