Hypoxanthine transport in the guinea pig and human placenta is a carrier-mediated process that does not involve nucleoside transporters.

Abstract

The purpose of this study was to characterize the mechanisms involved in the placental clearance of hypoxanthine. Uptake of isotope-labeled compounds was measured in the in situ perfused guinea pig placenta and in membrane vesicles isolated from the human syncytiotrophoblast. In the guinea pig hypoxanthine uptake (from the fetal circulation) proceeded by a saturable (Michaelis constant approximately 90 mumol/L), sodium-dependent mechanism that was inhibited by 19 mmol/L papaverine but not by 10 mumol/L nitrobenzylthioinosine or 10 mmol/L uridine. Uridine uptake was blocked by nitrobenzylthioinosine but not by papaverine or 4 mmol/L hypoxanthine. In human brush-border (maternal-facing) membrane vesicles hypoxanthine influx was sodium independent and best fitted to a saturable (Michaelis constant 290 +/- 45 mumol/L) plus a linear component. Saturable influx was blocked by papaverine but not by nitrobenzylthioinosine. Uridine uptake was not affected by 4 mmol/L hypoxanthine. Mediated hypoxanthine uptake by human basal (fetal-facing) membrane vesicles was not detected. At both placental blood-tissue interfaces hypoxanthine transport occurs through specific mechanisms that are different from the nucleoside transporters.