Calcium transport through the placenta

Abstract

The calcium content of the foetus increases exponentially during gestation. The transfer of calcium from the mother to the foetus is believed to occur via an active mechanism, based on observations that the calcium concentration is higher in foetal than in maternal blood, and that perfusion in situ of the umbilical artery of the placenta results in a net increase in the calcium concentration of the perfusate even when the calcium content of the perfusate is threefold higher than in the maternal blood. The calcium concentration in the foetal blood is mainly regulated by foetal parathyroid hormone and the plasma concentration of 1,25-(OH)2 vitamin D3. Several experiments suggest that this vitamin D metabolite plays a key role in calcium transport through the syncytial cell. A vitamin D dependent calcium binding protein has been detected in the placenta, which might intervene in the hormonal control of this transport. The cellular mechanisms of calcium transport through the placenta are not clearly defined. An ATP-dependent calcium uptake by microsomal membrane vesicles from human plancenta has been described by several investigators. This calcium transport is saturable, magnesium dependent, and displays Michaelis–Menten kinetics with a Km of approximately 70 nM ionized calcium. Two Ca2+ ATPases with low and high affinities for calcium are described. Since there are discrepancies concerning the exact localization of these enzymes in the syncytial cell, it has not been established whether they intervene in calcium transport through the placenta. Finally, the presence of adenylate cyclase in the basal plasma membrane, and a cAMP-dependent protein kinase in cytosol, microsomes, and brush border membranes, suggests, by analogy with the kidney, that this system might be involved in calcium transport. Further experiments are warranted to confirm this hypothesis.