Characterization of prostaglandin E1 transport in rat renal brush-border membrane

Transport of prostaglandin El (PGE(1)) was investigated in rat renal brush-border membrane vesicles. The uptake of[H-3]PGE(1) was sensitive to osmosis and temperature. This uptake was saturable and mediated by high-affinity (K-m = 2.1 mu M)/low-capacity (V-max = 17.4 pmol/mg protein/30 sec) and low-affinity (K-m = 526.5 mu M)/high-capacity (V-max = 1032.5 pmol/mg protein/30 sec) transport systems. [H-3]PGE(1) uptake was Na+-independent and inhibited by various eicosanoids including PGE(2) and PGF(2 alpha). Bromcresolgreen and sulfobromophthalein, potent inhibitors of prostaglandin transporter (PGT), significantly decreased [H-3]PGE(1) uptake. Uptake was also inhibited by indomethacin and probenecid, which reportedly have little effect on PGT. Benzylpenicillin and taurocholate decreased the uptake of [H-3]PGE(1). Like p-[C-14]aminohippurate (PAH) uptake by vesicles, the uptake of [H-3]PGE(1) was stimulated by an inside-positive membrane potential, created by applying an inward K+ gradient and valinomycin. However, the uptake of [H-3]PGE(1) was not inhibited by PAH, suggesting that PAH and PGE(1) are transported by separate transport systems. [H-3]PGE(1) uptake was not stimulated by outwardly directed gradients of Cl- nor unlabeled PGE(1), indicating that an anion exchanger may not be involved in PGE(1) transport. These findings suggest that the transport of PGE(1) in rat renal brush-border membrane is mediated by specific transport system(s), at least in part, by a potential-sensitive transport system.