Abstract

The hind paw, gracilis muscle, hind limb or kidney was perfused at constant blood flow in the anesthetized dog. Peripheral resistance changes in these vascular beds were determined by monitoring perfusion pressure. Two types of experiments were performed upon the perfused vascular bed. Angiotensin II amide was infused intraarterially in a very low dose into the hind paw or kidney and its influence on the vasoconstrictor response elicited during sympathetic stimulation was evaluated. In other experiments, angiotensin was administered in a range of doses into the carotid or vertebral artery and the changes in blood pressure and perfusion pressure were determined. The low dose of angiotensin infused intraarterially resulted in a significant increase, often great in magnitude, in the response to the sympathetic discharge in the cutaneous and renal vascular beds. No consistent vasoconstrictor response attributable to central stimulation was found in any of the vascular beds studied after the intracarotid or intravertebral injection of angiotensin. Barium chloride, administered by either the intracarotid or intravertebral route, produced vasoconstriction more consistently than did angiotensin. The vasoconstriction was centrally elicited, and was seen especially in muscle.