AJP - Renal Physiology, Vol 260, Issue 6 793-F799, Copyright © 1991 by American Physiological Society
Role of mineralocorticoids in adaptation of rabbit cortical collecting duct after loss of renal mass
V. M. Vehaskari and J. Herndon
Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri 63110.
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.
