Asymmetric calcium influx and efflux at maternal and fetal sides of the guinea‐pig placenta: kinetics and specificity.

Unidirectional influx of calcium across maternal and fetal sides of the syncytiotrophoblast was investigated in the guinea-pig placenta by using a rapid (less than 30 s) paired-tracer dilution technique. Experiments were performed in an in situ placenta artificially perfused through the umbilical vessels or in an isolated placenta in which both the maternal and fetal circulations were perfused. At equimolar Ca2+ concentrations, unidirectional calcium influx was always significantly lower on the maternal side than on the fetal side. Saturation kinetics were observed: on the fetal side the estimated Km was 1.8 +/- 0.7 mM and Vmax was 1.66 +/- 0.28 mumol/min X g (mean +/- S.E. of mean) and on the maternal side Km ranged from 0.18 to 1.15 mM and Vmax ranged from 0.12 to 0.59 mumol/min X g. When the inhibition of calcium influx was investigated on the fetal side of the trophoblast by using competing cations, the following sequence was observed: Ba2+ greater than Ca2+ congruent to Ni2+ greater than Sr2+ greater than Mg2+ congruent to Li+. Efflux of 45Ca2+ from the trophoblast into the ipsilateral circulation (backflux) was rapid (20-100% in 6 min) and asymmetric since the fetal:maternal ratio was 1.35 +/- 0.11 (mean +/- S.E. of mean) in the presence of 0.1 mM-Ca2+. In the dually perfused placenta, transplacental transfer (6 min) of 45Ca2+ varied over a wide range (0-80%); however, it was similar to that of the extracellular reference tracer, 22Na+, in either maternal-to-fetal or fetal-to-maternal directions. It is suggested that this is a consequence of the 'leakiness' of the dually perfused placenta since the transplacental transfer of 22Na+ and D-[3H]mannitol (or L-[14C]glucose) measured simultaneously were also variable but similar. Transplacental transfer of 45Ca2+ could not be used to characterize specific calcium-transport mechanisms, whereas highly sensitive trophoblast uptake measurements were provided by the single-circulation, paired-tracer technique. Our findings suggest the presence of a specific carrier-mediated transport system for calcium on both maternal and fetal surfaces of the trophoblast. The asymmetries in unidirectional influx into the trophoblast and rapid backflux indicate a mechanism by which the net transfer of calcium from the maternal to the fetal circulation is maintained in favour of the fetus.