Chronic renal failure is associated with impaired urine concentration. Previous studies have demonstrated that cortical collecting ducts (CCD) from uremic rabbits (with remnant kidneys) have an impaired response to arginine vasopressin (AVP). To determine whether this defect is an early, integral component of compensatory renal growth by the remnant kidney, we studied the response of CCD derived from rabbits one week after 75% nephrectomy. At one week, hypertrophy and adaptation in sodium transport are fully developed, but azotemia and interstitial fibrosis are absent. The animals with remnant kidneys failed to respond normally to water deprivation and dDAVP (maximum urine osmolality 738 +/- 29.1 mOsm/kg compared to 1378 +/- 207 in sham operated). However, in isolated, perfused CCD from remnant kidneys, AVP stimulated hydraulic water permeability to the same extent as in normal CCD or CCD from sham operated animals. AVP-induced cAMP generation per mm tubule length was significantly higher in the CCD from remnant kidneys (137.4 +/- 14.5 fmol/mm) than in the control group (82.4 +/- 11.9 fmol/mm), but not different when expressed per micrograms protein. These studies demonstrate that one week after reduction in renal mass there is no defect in the response of CCD to AVP, suggesting that the mechanisms responsible for the hyposthenuria after loss of renal mass are not related to any intrinsic cellular changes that occur in CCD early during compensatory renal growth.