The cause of death due to toxin F7, an angusticeps-type toxin, isolated from the venom of Dendroaspis angusticeps was studied in anesthetized mice. The carotid arterial blood pressure, the ECG and the respiratory movements were recorded. Within a few minutes after i.v. injection of F7 (1 mg/kg), both the rate and amplitude of the respiratory movements decreased and respiratory arrest took place within 15 min in most cases. Before respiratory arrest, marked bradycardia with various types of arrhythmia and oscillation of blood pressure were observed. Artificial ventilation could abolish these cardiovascular changes and maintain the blood pressure for a long period. Toxin F7 caused a transient and slight increase of arterial blood pressure which could be prevented by hexamethonium. Intracisternal application of F7 (1 mg/kg) caused a long-lasting hypertension and bradycardia and the respiratory arrest time was significantly longer than after i.v. injection. A large dose (50 mg/kg i.p.) of atropine, but not smaller doses (5-10 mg/kg), protected mice against respiratory failure induced by F7. In rats, the phrenic nerve discharge was prolonged during respiratory depression. Since F7 has a potent anticholinesterase activity, it is concluded that the respiratory failure induced by F7 is peripheral in origin, chiefly, if not entirely, due to its anticholinesterase activity.