AJP - Renal Physiology, Vol 259, Issue 3 458-F465, Copyright © 1990 by American Physiological Society
Acidification mechanisms on the basolateral membrane of renal vesicles from the developing nephron
M. Baum
Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas 75235.
The present study examined acidification mechanisms on the basolateral
membrane of the early renal vesicle, an undifferentiated ball of cells that
will develop into parts of the glomerulus, proximal tubule, loop of Henle,
and a portion of the distal convoluted tubule. Renal vesicles were
dissected from newborn rabbit kidneys and bathed in vitro. To examine the
basolateral membrane acidification mechanisms, intracellular pH (pHi) was
measured by use of the pH-sensitive dye
(2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein. Evidence for Cl(-)-base
exchange included the fact that removal of bath Cl-resulted in cell
alkalinization (7.35 +/- 0.03 to 7.48 +/- 0.05; P less than 0.01). Cell
alkalinization induced by Cl- removal was also observed in presence of a
voltage clamp without bath Na+ (7.18 +/- 0.02 to 7.39 +/- 0.04; P less than
0.01) and was inhibited by 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid
(DIDS). pHi recovery after acute alkalinization resulting from CO2 removal
was 0.20 +/- 0.03 pH units/min in the presence of Cl-, 0.07 +/- 0.01 in
experiments with 0.2 mM DIDS, and 0.07 +/- 0.01 in absence of bath Cl-. The
early renal vesicle also has a basolateral Na(+)-H+ antiporter. Removal of
bath Na+ resulted in cell acidification (7.36 +/- 0.09 to 7.18 +/- 0.06; P
less than 0.01), which was inhibited by 2 mM amiloride. Cell pH recovery
after acute acidification (NH4Cl prepulse technique) was entirely dependent
on bath Na+ and inhibited by amiloride. Thus the renal vesicle has
basolateral membrane Na(+)-H+ and Cl(-)-base exchangers that can defend
against cell acidification and alkalinization, respectively.
