AJP - Renal Physiology, Vol 250, Issue 3 419-F424, Copyright © 1986 by American Physiological Society
Electrogenic Na+-independent Pi transport in canine renal basolateral membrane vesicles
S. J. Schwab and M. R. Hammerman
To define the mechanism by which Pi exists from the renal proximal tubular
cell across the basolateral membrane, we measured 32Pi uptake in
basolateral membrane vesicles from dog kidney in the absence of Na+.
Preloading of basolateral vesicles with 2 mM Pi transstimulated 32Pi
uptake, which is consistent with counterflow. We used measurements of
transstimulation to quantitate the transport component of 32Pi uptake.
Transstimulation of 32Pi uptake was inhibited less than 30% by
concentrations of probenecid as high as 50 mM. In contrast,
transstimulation of 35SO4(2-) uptake by intravesicular SO4(2-) was
inhibited 92% by 5 mM probenecid. Preloading basolateral vesicles with
SO4(2-) did not result in transstimulation of 32Pi uptake. Accumulation of
32Pi in basolateral vesicles above steady state was driven by a membrane
potential (intravesicular positive), consistent with Na+-independent Pi
transport being accompanied by the net transfer of negative charge across
the membrane. We conclude that carrier-mediated, electrogenic
Na+-independent 32Pi transport can be demonstrated in basolateral vesicles
from dog kidney. This process appears to be mediated, at least in part, via
a mechanism different from that by which SO4(2-) is transported.
Electrogenic Na+-independent Pi transport may reflect one means by which Pi
reabsorbed across the luminal membrane exists from the proximal tubular
cell down an electrochemical gradient.
