Resting blood flow, arterio-venous glucose and oxygen (A-V)O2 differences, glucose uptake and oxygen consumption by a segment of the upper jejunum were measured in anaesthetized dogs. Systemic arterial pressure was also measured. The effect of nicotine infusion (25 micrograms kg-1 i.v., over 10 min) on these measurements was recorded in untreated dogs, in dogs treated with propranolol (0.5 mg kg-1) to produce beta-adrenoceptor blockade and in dogs after alpha 1-adrenoceptor blockade with prazosin (0.2 mg kg-1). Nicotine cause a significant pressor response during infusion and a hypotensive response during the post infusion period. Propranolol did not significantly affect these results. Jejunal blood flow increased in the first half of nicotine infusion in both the untreated and beta-blocked animals. Vascular resistance was reduced during nicotine infusion and the decrease persisted post infusion in the beta-blocked group. In the untreated group (A-V)O2 was significantly reduced during the first 5 min of nicotine infusion, thereafter it returned to control levels, then rose significantly above control level, post infusion. beta-Adrenoceptor blockade had little effect on these responses to nicotine. When oxygen consumption was calculated it was found that nicotine had little effect during or after infusion. Nicotine caused significant hyperglycaemia during and for about 1 h after infusion. Tissue release of glucose was occasionally observed following the infusion. beta-Adrenoceptor blockade reduced the hyperglycaemia caused by nicotine. beta-Blockade alone increased uptake and nicotine caused a further three to four fold increase. Prazosin abolished the effects that were observed in the untreated and the alpha-blocked animals. 6 The present findings, related to our previous observations on the effects of catecholamines on glucose uptake by the bowel, are consistent with the hypothesis that nicotine has its action on bowel glucose uptake or release through its well-established action in releasing catecholamines and in activating beta-adrenoceptors. The responses are not related to oxygen utilization.