Abstract

Transport of sulfate into brush border membrane (BBM) vesicles from renal tubules of southern flounder, Paralichthys lethostigma, was investigated. Imposition of a 21 mM HCO-3 gradient, in greater than out, produced concentrative sulfate uptake (overshoot) fourfold higher than equilibrium. Gradient conditions were necessary to produce this response; no overshoot was produced by the mere presence of HCO-3. Generation of potassium diffusion potentials with KCl gradients and valinomycin or short-circuiting of possible other ionic diffusion potentials had no effect on sulfate uptake. The rate-limiting step in HCO-3:SO2-4 exchange is, therefore, an electroneutral process. Although HCO-3 was the most effective counterion for sulfate, SCN-, Cl-, and S2O2-3 were also capable of promoting concentrative sulfate uptake. Sulfate uptake in the absence of counterion and bicarbonate-dependent sulfate uptake were both shown to be saturable processes. HCO-3-driven sulfate uptake could be inhibited by disulfonic stilbene, HgCl2, probenecid, chlorophenol red, and bromcresol green. Phloridzin, p-aminohippuric acid, 2,4-dinitrophenol, isethionic acid, and citric acid had no significant effect on HCO-3:SO2-4 exchange. The role of this sulfate:anion exchanger in active renal tubule sulfate secretion is discussed.

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