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Renal nerves were stimulated either directly (loop electrodes) or indirectly (bilateral carotid occlusion with maintenance of control blood pressure) in anesthetized dogs to determine the effects on renal blood flow (RBF), glomerular filtration rate (GFR), sodium excretion (UNaV), and intrarenal distribution of blood flow (microsphere method). Direct nerve stimulation decreased RBF 20% in 9 of 10 dogs; but GFR, UNaV, and intrarenal distribution of blood flow did not change significantly. Carotid occlusion decreased RBF in 9 of 10 dogs. There was a 22% fall in RBF for the whole group, GFR decreased 33%, and UNaV decreased from 0.39 to 0.17 muEq/min/g (p smaller than 0.05). A small (8%) decrease in midcortical fractional flow (p smaller than 0.05 after carotid occlusion was the only distributional flow change observed. The results disclosed no relationship between changes in sodium excretion and changes in total RBF, GFR, or intrarenal distribution of blood flow following nerve stimulation. These studies also indicate that the renal effects of carotid occlusion are probably not mediated by renal nerve stimulation alone.

The effect of acute renal denervation on renal blood flow (RBF) and intrarenal distribution of blood flow (microsphere method) was studied in dogs using three standard denervation models. Surgical denervation, by stripping renal vascular nerves and autoperfusing the kidney through a large bore plastic catheter, caused RBF and glomerular filtration rate to decrease. Also, intrarenal distribution of blood flow became asymmetric, that is, perfusion changes in the two halves of the kidney were not similar. Denervation by stripping away the neural tissue and infiltrating the hilum with 0.5% procaine and 50% ethanol produced no adverse effects on RBF, but distributional changes were asymmetric. Denervation by this method was probably incomplete as evidenced by decreased RBF following bilateral carotid occlusion. Intrarenal arterial infusion of 10 mug/kg/min phenoxybenzamine caused renal perfusion to change asymmetrically and did not abolish the decrease in RBF normally seen following nerve stimulation. Present results demonstrate denervation studies must be interpreted cautiously; because the denervation model may cause renal damage and asymmetric perfusion, and denervation may not be complete.