The role of renal sympathetic nerve activity in mediating the sodium retention of acute thoracic inferior vena cava constriction was studied in anesthetized dogs with clearance and micropuncture techniques. Combined saline loading and acute caval constriction in control dogs caused an antinatriuresis; there was no change in proximal fractional reabsorption. Maneuvers designed to interrupt renal sympathetic nerve traffic were applied to the left kidney: phenoxybenzamine, surgical renal denervation, and guanethidine. Each intervention resulted in an ipsilateral natriuresis and a fall in proximal fractional reabsorption. The ipsilateral natriuresis could not be explained by alterations in systemic or intrarenal hemodynamics or changes in the intrarenal distribution of blood flow or filtrate. The data provide evidence suggestive of a direct effect of the renal sympathetic nerves on tubular sodium transport.