Chronic Hypertension Elicited by Infusion of Angiotensin into Vertebral Arteries of Unanaesthetized Dogs

SUMMARY 1. Synthetic angiotensin I1 was infused chronically through catheters implanted into a vertebral artery and an external jugular vein of unanaesthetized dogs. Arterial pressure was recorded daily from an indwelling catheter in the abdominal aorta before, during and after the infusions. 2. Infusion of angiotensin 1 pg kg-' day-' into a vertebral artery caused mean arterial pressure to increase by an average of 12 mmHg in five dogs, and the rise was sustained throughout the infusion period of 7 days in all dogs. 3. When the infusion rate of angiotensin was increased to 10 pg kg-' day-', arterial pressure during vertebral artery infusion rose initially to a slightly greater extent but decreased at the end of the infusion, indicating tachyphylaxis. 4. During infusion of angiotensin into the vertebral circulation, arterial pressure rose rather than fell during sleep; awakening was accompanied by sharp fall in pressure. 5. It is concluded that there is an area in the central nervous system responsive to angiotensin that can cause a sustained rise in arterial pressure. Arterial pressure is increased in rabbits (Dickinson & Yu, 1967; Rosendorff, Lowe, Lavery & Cranston, 1970), dogs (Scroop & Lowe, 1969; Ferrario, Dickinson & McCubbin, 1970) and man (Ueda, Uchida, Ueda, Gondaira & Katayama, 1969) when angiotensin is infused into a vertebral artery in amounts that are ineffective when given intravenously. It is not known if this action of angiotensin is involved in the initiation, or maintenance, of renal hypertension. The experiments reported here were done to determine whether or not continuous infusion of small amounts of angiotensin into the vertebral arteries of unanaesthetized dogs could cause a rise in arterial pressure that would be sustained for days.