Reduction in Renal Vascular Responses to Angiotensin and Norepinephrine during Carotid Sinus Stimulation

In dogs anesthetized with morphine and chloralose, the renal vascular responses to angiotensin and norepinephrine were studied under conditions of altered sympathetic nervous activity. The kidneys and one or both carotid sinuses were perfused at a constant rate of flow. Sympathetic activity was altered by changing the mean carotid sinus perfusion pressure from approximately 30 to 200 mm Hg. During maximal carotid sinus pressure, the renal vasoconstrictor responses to angiotensin and norepinephrine were reduced by an average of 52% and 47%, respectively. Similar results were obtained in innervated, chronically denervated, and excised kidneys perfused with the dogs' own blood. Increasing carotid sinus pressure alters the responsiveness of the renal vasculature to angiotensin and norepinephrine by some mechanism that is not dependent on the renal sympathetic nerves or on norepinephrine. It is proposed that raising mean carotid sinus pressure alters the concentration of some bloodborne substance and so reduces the vasoconstrictor responses to these vasoactive agents in the renal vascular bed.