Characterization of Prostaglandin E1 Transport in Rat Renal Brush-border Membrane

Summary:Transport of prostaglandin E1 (PGE1) was investigated in rat renal brush-border membrane vesicles. The uptake of [3 H]PGE1 was sensitive to osmosis and temperature. This uptake was saturable and mediated by high-affinity (Km = 2.1 μM)/low-capacity (Vmax = 17.4 pmol/mg protein/30 sec) and low-affinity (Km = 526.5 μM)/high-capacity (Vmax = 1032.5 pmol/mg protein/30 sec) transport systems. [3H]PGE1 uptake was Na+-independent and inhibited by various eicosanoids including PGE2 and PGF2α. Bromcresol green and sulfobromophthalein, potent inhibitors of prostaglandin transporter (PGT), significantly decreased [3H]PGE1 uptake. Uptake was also inhibited by indomethacin and probenecid, which reportedly have little effect on PGT. Benzylpenicillin and taurocholate decreased the uptake of [3H]PGE1. Like p-[14C]aminohippurate (PAH) uptake by vesicles, the uptake of [3H]PGE1 was stimulated by an inside-positive membrane potential, created by applying an inward K+ gradient and valinomycin. However, the uptake of [3H]PGE1 was not inhibited by PAH, suggesting that PAH and PGE1 are transported by separate transport systems. [3H]PGE1 uptake was not stimulated by outwardly directed gradients of Cl– nor unlabeled PGE1, indicating that an anion exchanger may not be involved in PGE1 transport. These findings suggest that the transport of PGE1 in rat renal brush-border membrane is mediated by specific transport system(s), at least in part, by a potential-sensitive transport system.