Effect of Parathyroid Hormone on PO4 Transport through the Human Placenta Microvilli

Abstract

The transport of phosphate (PO₄) through the placenta is a secondary active phenomenon whose control mechanisms are unknown. In this study, we investigated whether PTH, the main hormone regulating PO₄ transport in the kidney and gut, has a similar role in the placenta. Incubation of normal term human placenta fragments for 1 min with PTH increased the cAMP content of the tissue by 285%. A dose-response curve of the effect of the hormone showed that the cAMP accumulation reached a maximal level with 3.5 x 10^-8 M PTH. Incubation of the placenta fragments with 10^-4 M di-butyryl cAMP resulted in a significant decrease in the PO₄ uptake by the brush border membranes prepared from these fragments. Increasing concentrations of di-butyryl cAMP from 0 to 10^-3 M significantly decreased the PO₄ uptake from 0.29 ± 0.02 to 0.22 ± 0.01 pmol/μg/20 s. Similarly, incubation of the placental tissue with PTH resulted in a comparable decrease in the PO₄ uptake by the corresponding brush border membrane vesicles. In contrast, direct incubation of brush border membranes with the hormone did not influence PO₄ uptake. It is concluded that PTH probably regulates the PO₄ transport through the placenta syncytiotrophoblast cell through cAMP mediation. Because adenylate cyclase is located in the basal plasma membrane, it is likely that only the fetal hormone is implicated in this process