In anaesthetized and artificially ventilated rabbits an intravenous infusion of paraoxon (0.8 mg/kg) was given over 30 min. The effects on cardiac output, blood flow to various vascular beds, and on the mass discharge of the postganglionic sympathetic efferents to the spleen and kidney were monitored. Immediately following paraoxon infusion atropine (0.5 mg/kg) was injected intravenously. Within 20 min of commencing the infusion signs of increased cholinergic stimulation were observed. Between the 20th and 25th min mean arterial blood pressure, heart rate, and cardiac output fell markedly. Even before arterial blood pressure fell total peripheral resistance and regional resistance to flow through the subclavian and coeliac arteries increased significantly, whereas resistance was below control, increased regional resistance being found only in the vascular beds of the subclavian and splenic arteries. The activity in the splenic sympathetic efferents increased, while the activity in the renal efferents was sharply reduced. While an effective antidote, atropine elicited transient intestinal vasodilation and a further transient decrease in total peripheral resistance. These and other results suggest that muscarinic mechanisms are mainly responsible for the paraoxon-induced changes in regional blood flow and regional sympathetic activity. The vasodilatory effect of atropine in the intestine was probably due to a local autoregulatory mechanism.