Abstract
The role of the kidney in foetal erythropoiesis was studied in newborn SD mice on the day of birth. Some of the homozygotes and heterozygotes of this strain are born anephric. Red cell production was evaluated by haematocrit levels, reticulocyte counts, and Fe59-uptake in liver and RBC, the isotope given to the mothers during pregnancy. Erythropoiesis of the newborn with renal agenesis was not different from that of animals with intact kidneys. When the mothers were exposed to hypoxia during pregnancy, significantly higher haematocrit- and reticulocyte levels were observed, and there was no difference in erythropoiesis of anephric newborn compared with newborn with intact kidneys. Red cell production was also similar in those with and without kidneys when the mothers were hypertransfused. Plasma erythropoietin levels in the offspring of normal pregnancies were determined. Detectable concentrations of the hormone were found, and the levels were the same in anephric and normal newborn. Exposure to hypoxia (0-5 atm for 6 h) significantly increased plasma erythropoietin levels. This increase was of the same magnitude in animals with and without kidneys. This study indicates that murine foetal erythropoiesis is regulated by erythropoietin in the same way as later in life. Since abolition of the erythropoiesis of the mothers through hypertransfusion, did not influence the red cell production of the foetuses, Ep seems not to cross placenta. Erythropoietin is, therefore, produced extrarenally during this period.