The role of vitamin D in regulating placental transport of calcium and phosphate in pigs was studied using the "Hannover Pig Strain" which suffers from pseudo-vitamin D-deficiency rickets, type I. Sows and fetuses of normal phenotype (heterozygotes) and of homozygote phenotype which suffered from clinical symptoms of rickets were used. The homozygote animals are devoid of renal 25-cholecalciferol-1-hydroxylase. In the rachitic sows which normally depend on treatment with pharmacological doses of vitamin D3 at intervals of four to six weeks, vitamin D-treatment was discontinued two months before conception. Ca, P and 1.25-(OH)2D3 concentrations in plasma of sows and fetuses (Aa. umb., V. umb.) were measured in samples obtained at term during cesarian section. Mean concentrations of Ca and P in heterozygote sows at parturition were 2.34 mmol/l and 2.33 mmol/l, respectively, and were significantly higher than in homozygote sows, 1.58 mmol/l and 1.26 mmol/l, respectively. Ca concentrations in plasma of the umbilical vein of fetuses from both homozygote and heterozygote sows were normal, however, (3.23 mmol/l and 2.96 mmol/l, respectively) and statistically not different from each other. No significantly different P concentrations in arterial plasma of fetuses from heterozygote or homozygote sows were seen, either. The concentrations of Ca and P in the arterial umbilical plasma were significantly higher (p less than 0.001) than in venous plasma of both homozygote and heterozygote fetuses, indicating net placental transfer of these elements in both genotypes. The concentration of 1.25-(OH)2D3 in hypocalcemic sows at term (25.5 +/- 8.25 pg/ml) was significantly lower than that in the normocalcemic (heterozygote) sows (84.1 +/- 25.6 pg/ml). The 1.25-(OH)2D3 concentration in arterial plasma of fetuses from homozygote sows was only 46% that of fetuses from normocalcemic sows which showed transfer of calcitriol from mother to fetus. It is concluded from these studies that in pigs, renal production and physiological concentrations of 1.25-(OH)2D3 in either mother or fetus is not essential for the maintainance of the Ca and P homeostasis in the fetal-maternal system.