Mueller, I.I.MuellerHagos, YohannesYohannesHagosBurckhardt, GerhardGerhardBurckhardtBurckhardt, Birgitta-ChristinaBirgitta-ChristinaBurckhardt2018-11-072018-11-072005https://resolver.sub.uni-goettingen.de/purl?gro-2/49637Renal elimination of drugs bound to plasma proteins is mediated mainly by tubular secretion. Furosemide, a frequently used diuretic, is tightly bound to plasma proteins and is believed to be secreted. It contains a carboxyl group and a sulfamoyl moiety and may therefore be a substrate for the sodium-dependent dicarboxylate cotransporter from human kidney (hNaDC-3). Furosemide, besides inhibiting [C-14]succinate uptake, reduced succinate-associated currents in a dose-dependent manner with an IC50 of 2.2 mM. Furosemide showed sodium-dependent inward currents as evidence for its translocation by hNaDC-3. The concentrations necessary to affect hNaDC-3, however, are far higher than the therapeutically relevant plasma concentrations of furosemide. This implies that dicarboxylate uptake necessary for drug excretion via organic anion/dicarboxylate exchange will not be altered by therapeutical doses of furosemide.journal_article10.2174/157018005774479087000235168000013