Renal hemodynamics and neurophysiologic techniques were used to evaluate the role of the renal nerves in the compensatory adaptation to ureteral occlusion in anesthetized dogs. Left ureteral occlusion produced ipsilateral renal vasodilatation (left renal blood flow increased from 315 .+-. 28-362 .+-. 33 ml/min) and contralateral vasoconstriction (right renal blood flow decreased from 331 .+-. 23-273 .+-. 19 ml/min). Afferent renal nerve activity from the ipsilateral, vasodilating kidney increased from 6.1 .+-. 0.3-8.5 .+-. 0.5 Hz and efferent renal nerve activity to the contralateral, vasoconstricting kidney increased from 7.4-10.1 .+-. 1.0 Hz. Functionally verified surgical denervation of either kidney abolished the contralateral renal vasoconstrictor response to ureteral occlusion, whereas the ipsilateral renal vasodilator response was unaffected. Transection of the spinal cord at T6 (6th thoracic) did not affect the ipsilateral renal vasodilator response but abolished the contralateral renal vasoconstrictor response to ureteral occlusion. Ureteral occlusion evidently produces reflex vasoconstriction in the contralateral kidney. The afferent signal derives from the occluded kidney and travels via afferent renal nerve fibers to the spinal cord with central connections above T6; the efferent limb is via efferent renal sympathetic nerve fibers.