The effect of angiotensin II on heart rate of dogs were studied by intravenous and intracerebroventricular routes. Following differences were noticeable when the results obtained with intracerebroventricular were compared with those obtained after intravenous administration. The onset of tachycardia was less as compared to the intravenously administered angiotensin. The dogs required to produce tachycardia was less and the magnitude of tachycardia was also greater with intracerebroventricular administration. The initial bradycardia observed with intracerebroventricular or intravenous administration of angiotensin, could be prevented by using the mechanical buffering device. The spinal cord transection at C2 level and bilateral vagotomy abolished the tachycardia. It is speculated that angiotensin acts centrally either on the hypothalamic or medullary accelerator neurones (central sympathetic structures) and produces some degree of increased adrenegic neuron discharge which is responsible for cardiac acceleratin in dogs.