Angiotensin II (Ang II) is known to activate central sympathetic neurons. In this study we determined the effects of Ang II on the autonomic components of the cardiovascular responses to stimulation of nasopharyngeal receptors with cigarette smoke. Experiments were carried out in conscious New Zealand white rabbits instrumented to record arterial pressure and heart rate. Rabbits were exposed to 50 cc cigarette smoke before and after subcutaneous osmotic minipump delivery of Ang II at a dose of 50 ng/kg/min for one week in one group and intracerebroventricular (ICV) infusion at a dose of 100 pM/min for one hour in a second group. The responses were compared prior to and after heart rate was controlled by pacing. Autonomic components were evaluated by intravenous administration of atropine methyl bromide (0.2 mg/kg) and prazosin (0.5 mg/kg). Ang II given either systemically or ICV significantly blunted the pressor response to smoke (p<0.05) when the bradycardic response was prevented. This blunted response was not due to an absolute increase in baseline blood pressure post Ang II infusion (71.64 ± 11.6 vs 92.1 ± 19.8, p<0.05) since normalization of blood pressure with sodium nitroprusside to pre Ang II levels also resulted in a significantly blunted pressor response to smoke. The effect of smoke was 1-adrenergic receptor-mediated since it was essentially abolished by prazosin in both the pre and the post Ang II states (p<0.05). These results suggest that elevations in central Ang II reduce the sympathetic response to smoke in conscious rabbits. This effect may be due to an augmentation of baseline sympathetic outflow and a reduction in reflex sensitivity similar to the effect of Ang II on baroreflex function.