The weak neurotoxin from the Naja kaouthia cobra venom was found to reduce, under the intravenous administration to rats, the arterial blood pressure and increase the heart rate.
We studied the effects of blockade of nicotinic receptors in sympathetic and parasympathetic ganglia (hexamethonium), muscarinic receptors (atropine), and beta1-adrenoceptors (atenolol) on arrhythmogenic activity of endothelin-1 during inhibition of nitric oxide synthesis with Nomega-nitro-L-arginine in NMRI mice. Atropine reduced, while hexamethonium completely abolished the arrhythmogenic effect of endothelin-1 during nitric oxide synthase inhibition. Atenolol potentiated arrhythmogenic activity of Nomega-nitro-L-arginine, but endothelin-1 had no effect on the incidence of arrhythmias under these conditions.
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