Increased sodium transport by cortical collecting tubules from remnant kidneys.

To determine whether intrinsic changes in cortical collecting tubule (CCT) transport contribute to the maintenance of sodium and acid-base balance after loss of renal mass, we studied transport functions in isolated perfused CCT from rabbit remnant kidneys. The rabbits were sacrificed three weeks after surgical reduction of renal mass (by 3/4 to 7/8) at which time they were mildly azotemic but had no systemic electrolyte or acid-base disturbances. When perfused by standard methods in vitro, CCT from remnant kidneys exhibited sodium transport rates (lumen-to-bath 22Na-flux) approximately twice as high as those in CCT from control animals (111 +/- 19 vs. 54 +/- 7 pmol/min mm, P less than 0.02). A similar difference was present in the ouabain-sensitive sodium fluxes (81 +/- 16 vs. 39 +/- 8 pmol/min mm, P less than 0.05). In contrast, there were no significant differences in net bicarbonate transport. Significant hypertrophy of the remnant kidney CCT was reflected by 30 to 45% increases in tubule diameters. To examine the possible role of differences in food intake, we studied a separate group of weight-matched, pair-fed sham-operated and remnant kidney rabbits. Similar differences in total and ouabain-sensitive 22Na-flux, and in tubule size persisted in the pair-fed animals. A dissociation between active sodium transport and tubule hypertrophy was documented in the outer medullary collecting tubule: despite the lack of active sodium transport, hypertrophy was present. Our studies show that loss of renal mass results in a selective augmentation of certain transport processes in the CCT, implying selective or specific signals and mechanisms.