E. Brandle et al., IN-SITU CHARACTERIZATION OF OXALATE TRANSPORT ACROSS THE BASOLATERAL MEMBRANE OF THE PROXIMAL TUBULE, Pflugers Archiv, 435(6), 1998, pp. 840-849
Oxalate transport across the contraluminal membrane of the proximal tu
bule was studied in vivo using the ''capillary stopped flow microperfu
sion method'' (Pflugers Arch 400:250-256, 1984). Cellular uptake of ox
alate was characteristic of a carrier-mediated transport process (J(ma
x) = 1.6 +/- 0.6 pmol/s per cm proximal tubular length, K-m = 2.03 +/-
0.77 mmol/l). Sulphate inhibited oxalate transport in a dose-dependen
t manner (K-i-value = 1.53 +/- 0.38 mmol/l). Sulphate transport across
the basolateral membrane was also characteristic of a carrier-mediate
d transport process (J(max) = 1.83 +/- 0.56 pmol/s per cm proximal tub
ular length, K-m = 1.37 +/- 0.57 mmol/l). Oxalate inhibited the sulpha
te transport in a dose-dependent manner (K-i = 2.06 +/- 0.82 mmol/l).
No significant differences were found between the K-i values and the K
-m values of the two substances, indicating that oxalate and sulphate
are transported by the same carrier across the basolateral membrane of
the proximal tubule. Oxalate transport was not dependent on the extra
cellular sodium or potassium concentration. Bicarbonate competitively
inhibited the oxalate transport. Chloride significantly inhibited the
oxalate transport, but not dose dependently. It is, therefore, suggest
ed that oxalate is transported into the cell of the proximal tubule in
exchange for sulphate or bicarbonate. The dose-independent inhibition
by chloride is suggested to be mediated by the coupling of the sulpha
te (bicarbonate)/oxalate exchanger with the chloride/bicarbonate excha
nger at the basolateral membrane of the proximal tubule. This, further
more, suggests that the transport of oxalate or sulphate across the ba
solateral membrane might be indirectly coupled with the reabsorption o
f chloride at this membrane side.