Endocrine Regulation of Plasma Phosphate in Sheep Fetuses with Catheters Implanted in utero
Before term, in rodents (1, 2), ruminants (3, 4, 5, 6) and humans (7), phosphatemia is higher in the fetus than in the mother. This difference of concentration between both sides of the placenta is poorly understood. In rats, it has been demonstrated that the placental transfer of 32P increased between the 19th day of gestation and term (1). In the same time fetal phosphatemia increased from 8.75 to 9.97 mg/dl (2). Calcitonin injection in fetal rats (8) and in fetal monkeys (9) induced a significant hypocalcemia and hypophosphatemia in the fetus. In rat fetuses treated with parathyroid extract intravenously or subcutaneously calcemia was increased while phosphatemia was lower than in fetuses injected with the vehicle alone (10). In acute preparations of sheep fetuses, the intravenous infusion of parathyroid extract (0.1 I.U./kg/mn during 1 hr) increased promptly and significantly the renal phosphate-glomerular filtration rate clearance ratio, while the glomerular filtration rate, serum calcium, serum phosphate and filtered load of phosphate did not change significantly (4). In fact the endocrine regulation of fetal phosphatemia remains obscure.The purpose of this investigation was to study the effects of calcitonin, parathyroid hormone, 1α-hydroxycholecalciferol and 5,6 trans-25 hydroxycholecalciferol, injected intravenously in unstressed fetal lambs, on fetal and maternal phosphatemia, calcemia and magnesemia.
KeywordsEndocrine Regulation Maternal Plasma Salmon Calcitonin Fetal Plasma Plasma Phosphate
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