Electrogenic H(+)-regulated sulfate-chloride exchange in lobster hepatopancreatic brush-border membrane vesicles.

Transport of [35S]sulfate by brush-border membrane vesicles (BBMV) of lobster (Homarus americanus) hepatopancreas was stimulated by an outwardly directed chloride gradient. In contrast, sulfate uptake was not enhanced by inwardly directed Na+ or K+ transmembrane gradients. An inside-positive membrane potential (valinomycin and K+) stimulated SO4(2-)-Cl- exchange, whereas an inside-negative membrane potential was inhibitory. Sulfate-sulfate exchange was not affected by alterations of transmembrane potential. An inwardly directed proton gradient, or the presence of low bilateral pH, enhanced SO4(2-)-Cl- exchange, but the H+ gradient alone did not stimulate sulfate uptake in chloride-equilibrated BBMV or in vesicles lacking internal Cl-. The stilbenes 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS) and 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) strongly inhibited SO4(2-)-Cl- exchange. Sulfate influx occurred by a combination of carrier-mediated transfer, exhibiting Michaelis-Menten kinetics, and nonsaturable "apparent diffusion." 36Cl- influx into sulfate-loaded BBMV was stimulated by an inside-negative transmembrane potential compared with short-circuited vesicles. These results suggest that sulfate-chloride exchange in hepatopancreatic BBMV occurred by an electrogenic carrier mechanism exhibiting a 1:1 flux ratio that was modulated by internal and external H(+)-sensitive regulatory sites. The role of this antiport process in anion secretion is discussed.