Sulfate-bicarbonate exchange in brush-border membranes from rat renal cortex.
Under Na+-free conditions, SO4(2-) uptake by rat renal brush-border membrane (BBM) vesicles could be driven by imposition of a HCO3- gradient (in greater than out). The initial rate of SO4(2-) uptake was stimulated 10-fold, and peak overshoot exceeded equilibrium uptake by 2-3 times. Cl-, SCN-, NO3-, I-, and OH- were able to substitute for HCO3-. Divalent anions, including SO4(2-) itself, were less effective as counterions. Similarly, in the absence of Na+,SO4(2-) efflux was stimulated most effectively by the monovalent ions. HCO3- -SO4(2-) exchange was cis-inhibited by disulfonic stilbenes [4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS), 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS)], phloretin, Hg, and S2O3(2-). HCO3- driven SO4(2-) uptake was saturable, with an apparent Km of 0.4 mM for SO4(2-). Simultaneous imposition of Na+ (out greater than in) and HCO3- (in greater than out) gradients produced approximately additive stimulation of SO4(2-) uptake. The HCO3- -driven component of SO4(2-) uptake, but not the component driven by Na+, was inhibited by SITS. Finally, Na+-driven SO4(2-) accumulation could be reduced by imposing an out greater than in HCO3- gradient, conditions accelerating exchange driven SO4(2-) efflux. These findings indicate the presence of separate Na+-SO4(2-) cotransport and SO4(2-)-anion exchange pathways in the same BBM vesicles.
D000818:Animals; D000838:Anions / Q000494:pharmacology; D001639:Bicarbonates / Q000378:metabolism* / Q000494:pharmacology; D001692:Biological Transport; D007474:Ion Exchange; D007672:Kidney Cortex / Q000378:metabolism* / Q000648:ultrastructure; D007700:Kinetics; D008871:Microvilli / Q000378:metabolism; D051381:Rats; D012964:Sodium / Q000378:metabolism / Q000494:pharmacology; D013431:Sulfates / Q000037:antagonists & inhibitors / Q000378:metabolism*
D000838:Anions; D001639:Bicarbonates; D013431:Sulfates; D012964:Sodium