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Substrate Specificity of an H+/quinidine Antiport System in Human Embryonic Kidney HEK293 Cells

We recently found the H + /quinidine (QND) antiport system in canine kidney MDCK and porcine kidney LLC-PK 1 cells. The aims of the present study were to confirm the presence of the H + /QND antiport system in human embryonic kidney (HEK) 293 cells, and to investigate the substrate specificity of the system. The cellular uptake of 100 µ M QND into HEK293 cells was decreased by acidification of extracellular pH and by NH 4 Cl-induced alkalization of intracellular pH. In addition, a lipophilic cationic drug, diphenhydramine (DPH), significantly decreased the QND uptake in HEK293 cells. In order to evaluate the substrate specificity of the renal H + /QND antiport system, we investigated the DPH-sensitive uptake ( Δ uptake) of 12 cationic compounds (celiprolol, acebutolol, procainamide, pindolol, bisoprolol, metoprolol, flecainide, clonidine, pyrilamine, QND, propranolol, and verapamil). The Δ uptake positively correlated with their lipophilicity (Log D) values, and negatively correlated with their polar surface area (Log PSA) values. In contrast, the Δ uptake did not correlate with their molar volume (MV), molar refractivity (MR), or polarization (PO). These findings indicate that an H + /QND antiport system is present in HEK293 cells, and that the Log D and Log PSA of drugs are important factors responsible for the transport activity of the postulated H + /lipophilic cation antiporter in the kidney.