Complementary to its essential role in the central nervous control of cardiovascular activity, the neuropeptide angiotensin II may regulate attentional processes. The present study evaluated central nervous, cardiovascular, and sympathetic indicators of attention after inhibition of angiotensin II synthesis by captopril (50 mg vs. placebo) in 14 men. Event-related potentials (ERPs) and stimulus-related electroencephalographic (EEG) activity were recorded while the subject performed an auditory oddball task. Captopril increased both the N1-P2 component of the ERP (p < .05) and--following the first tone of the task--the EEG desynchronization in the lower alpha frequency band (p < .05). Although blood pressure remained unchanged, heart rate was lowered (p < .05) and plasma norepinephrine concentrations increased (p < .01) after captopril. The effects suggest that inhibition of angiotensin II synthesis enhances an attentional state typically present during sensory intake.