Abstract
Transport of prostaglandin E1 (PGE1) was investigated in rat renal brush-border membrane vesicles. The uptake of [3H]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.