Abstract
Cord blood plasma has high concentrations of estrone (E1), estradiol (E2) and estriol (E3). E2 causes hypocalcemia in newborn rats and in parathyroidectomized (PTX) adults. Since kidney and intestine have been excluded as sites of this action, bone is the presumptive locus of calcium (Ca) sequestration.
Uniform discs from the calvaria of newborn rats and young mice were incubated in Krebs' solution. The addition of E2 to the medium or prior E2 injection of the donors increased Ca uptake by 60-100%. Nitromiphene, a competitive blocker of estradiol, prevented this effect and eliminated hypocalcemia after E2 in vivo. Discs from donors injected with parathyroid extract (PTE) showed decreased Ca uptake; when both PTE and E2 were given, uptake equalled that of uninjected controls. Since E2 lowers Ca in PTX rats. Its effect on bone must be independent of, as well as opposite to, that of parathyroid hormone.
E1, thought to be active only after hepatic conversion to E2, caused hypocalcemia in vivo but not in vitro. E3 was inert both in vivo and in vitro.
These findings suggest that the high plasma estrogen concentrations present in the neonate may contribute to hypocalcemia through a direct effect on bone.
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Bergstrom, W., Jacobs, R. & Williams, M. ESTROGEN EFFECT ON CALCIUM UPTAKE BY BONE. Pediatr Res 11, 511 (1977). https://doi.org/10.1203/00006450-197704000-00848
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DOI: https://doi.org/10.1203/00006450-197704000-00848