Neural and angiotensin-mediated influences that alter hemodynamic and excretory behavior of the nonclipped kidney of two-kidney, one clip hypertensive rats were assessed by sequential acute surgical denervation of the nonclipped kidney and intravenous infusion of converting enzyme inhibitor (SQ 20881), 3 mg/kg hr. Normal and two-kidney, one clip hypertensive rats (0.2-mm silver clip on the right renal artery 3–4 weeks before study) were prepared to allow study of each kidney. Mean arterial blood pressure of two-kidney, one clip hypertensive rats fell significantly from control values of 149 ± 6 to 135 ± 6 mm Hg after denervation of the nonclipped kidney. Despite this decrease in arterial pressure, the nonclipped kidney exhibited significant increases in glomerular filtration rate (from 1.00 ± 0.08 to 1.24 ± 0.08 ml/min), sodium excretion (from 88 ± 39 to 777 ± 207 nEq/min), fractional sodium excretion (from 0.06 ± 0.02 to 0.54 ± 0.14%), and urine flow rate (from 3.7 ± 0.5 to 8.2 ±1.1 fiVmin). A significant decrease in glomerular filtration rate (from 1.12 ± 0.07 to 0.85 ± 0.08 ml/min) with no change in excretory function was observed for the clipped kidney following denervation of the nonclipped kidney. Intravenous addition of converting enzyme inhibitor significantly increased renal blood flow (from 7.0 ± 1.3 to 10.6 ± 1.5 ml/min) and sodium excretion (from 777 ± 207 to 1384 ± 425 nEq/min) for the nonclipped kidney; blood pressure decreased from 135 ± 6 to 123 ± 4 mm Hg, and renal vascular resistance decreased significantly (from 22 ± 3 to 13 ± 2 mm Hg -min/ml). In normal rats acute surgical denervation of one kidney resulted in reductions in arterial pressure and ipsilateral increases in urine flow rate and sodium and potassium excretion that were of smaller magnitude than those observed in the denervated kidney of the two-kidney, one clip hypertensive rats; sodium excretion decreased slightly in the untouched, innervated kidney. Addition of converting enzyme inhibitor produced a further increase of sodium excretion hi both kidneys. Renal hemodynamics were not altered in either kidney throughout the experiment. These results suggest that renal neural influences, in addition to angiotensin-mediated effects, contribute to the altered hemodynamic and excretory behavior of the nonclipped kidney of the two-kidney, one clip hypertensive rat.