The role of sympathetic nerves and circulating catecholamines in mediating the renal vascular response to severe exercise was examined in normal dogs and dogs with experimental heart failure, using paired normal and denervated kidneys. In normal dogs, mean arterial blood pressure increased gradually from 97 ± 4 to 137 ± 6 mm Hg, renal blood flow remained at control levels, and renal vascular resistance rose from 0.57 ± 0.04 to 0.84 ± 0.15 mm Hg/ml min^-1 during peak steady-state exercise. The increase in resistance was similar in the denervated renal bed and persisted after alpha-receptor blockade. Exercise in dogs with heart failure increased mean arterial blood pressure slightly from 103 ± 4 to 111 ± 5 mm Hg. In the innervated kidney, blood flow dropped precipitously from 148 ± 6 to 46 ± 9 ml/min, and renal resistance increased from 0.73 ± 0.08 to 3.35 ± 0.53 mm Hg/ml min^-1. In the denervated kidney, renal blood flow decreased from 174 ± 12 to 120 ± 1 ml/min, and resistance increased from 0.59 ± 0.07 to 0.94 ± 0.09 mm Hg/ml min^-1. After alpha-receptor blockade, the decrease in flow and the increase in resistance to the denervated kidney were further attenuated. Thus, in normal, healthy dogs, the contribution of adrenergic mechanisms to renal vascular regulation appears to be minimal; blood flow remains constant in the presence of elevated pressure, suggesting that autoregulation is responsible for the elevated renal resistance during exercise. In dogs with experimental heart failure, intense renal sympathetic vasoconstriction prevails throughout exercise; the major portion of this response is neurally mediated, with an additional contribution by circulating catecholamines.