Abstract
Mechanisms of transfer of inorganic phosphate, Pi, across the placenta of rats at 21 days of gestation were studied using (32)Pi. In one group of experiments the unidirectional transfer of Pi from mother to fetus was estimated from radioactivity in the fetus at various intervals after the tracer injection into the mother.
At 15 min after tracer injection, the transfer rate was only slightly higher than the estimated rate of fetal accretion of Pi, and it decreased rapidly with the length of the experiment suggesting deterioration of the transfer mechanism under conditions of an acute experiment. In other experiments, transfer of (32)pi and Cr-51-EDTA (a marker of paracellular transfer) were measured across the dually-perfused placenta in the maternal-fetal direction.
The transfer rate of (32)pi was,, order of magnitude higher than the transfer of Cr-51-EDTA indicating that most of the Pi transfer is transcellular. The transfer of P-32 decreased when the concentration of Na+ in the maternal perfusate was reduced, it was related inversely to the concentration of Pi on the fetal side of the placenta, and it was related directly to the concentration of Ca2+ on the fetal side.
The maternal-fetal transfer of Pi exhibited saturation kinetics with a K-m, of about 0.4 mM suggesting that at a physiological concentration of Pi in maternal plasma the transfer mechanism is nearly saturated. The present observations are consistent with Pi being transferred in cotransport with Na+.
The maternal-fetal transport of Pi appears to be stabilized by the high affinity of the transport system to Pi, and controlled by a negative feedback between fetal concentration of Pi and the Pi transfer rate. It may also be controlled, to some degree, by the fetal plasma Ca2+.