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We studied the effect of the venom of the Brazilian spider, Lasiodora sp. (Mygalomorphae, Theraphosidae), on force generation and electrical activity in the isolated rat heart. Previous work showed that this venom is excitotoxic to excitable cells due to Na+ channel gating modifier activity [Toxicon 39 (2001) 991]. In the isolated heart, the venom (10–100 μg bolus administration) caused a dose-dependent bradycardia, with transient cardiac arrest and rhythm disturbances. The electrocardiogram showed that the reduction of heart rate was due to sinus bradycardia, sinus arrest and partial or complete A–V block. All of the effects were reversible upon washout of the venom. The effect of the venom was potentiated by the anticholinesterase neostigmine (3.3 μM), suppressed by the muscarinic acetylcholine receptor antagonist atropine (1.4 μM), and inhibited by the vesicular acetylcholine transporter inhibitor (−)-vesamicol (10 μM). Tetrodotoxin (200 nM) did not inhibit the effect of the venom. Together, these data suggest that this Lasiodora venom evokes vesicular release of acetylcholine from parasympathetic nerve terminals by activating tetrodotoxin-resistant Na+ channels. [Copyright &y& Elsevier]