Role of mineralocorticoids in adaptation of rabbit cortical collecting duct after loss of renal mass.

The mechanism of compensatory adaptation and hypertrophy of the cortical collecting duct (CCD) was studied by in vitro microperfusion technique after surgical loss of functioning nephrons in the rabbit. Sodium transport was increased at 1 wk (lumen-to-bath sodium transport of 127 +2- 9 vs. 61 +/- 11 pmol.mm-1.min-1 in sham-operated animals, P less than 0.01) and 3 wk (111 +/- 19 vs. 54 +/- 7 pmol.mm-1.min-1, P less than 0.05) but not 16 h (81 +/- 13 vs. 78 +/- 8 pmol.mm-1.min-1) after loss of renal mass. The functional adaptation was accompanied by an increase in the size of the CCD. A rise in plasma aldosterone levels preceded and accompanied the increased sodium transport rate. Adrenalectomy at the time of reduction of renal mass totally prevented the development of both hypertrophy and sodium transport adaptation (sodium transport 15 +/- 8 pmol.mm-1.min-1). When adrenalectomy was combined with clamping the plasma aldosterone level in the nonstressed physiological range, compensatory hypertrophy and adaptation also failed to develop (sodium transport, 66 +/- 10 pmol.mm-1.min-1), but with high-dose aldosterone replacement both the hypertrophy and adaptation of sodium transport (130 +/- 23 pmol.mm-1.min-1) were restored. The results document the importance of increased mineralocorticoid activity in the development of compensatory hypertrophy and adaptation of sodium transport in rabbit CCD after loss of renal mass.