Calcium ‘homeostatic’ effect of 1α,25-dihydroxycholecal-ciferol on young adult mouse calvaria in organ culture

Abstract

The effect of 1α,25-dihydroxycholecalciferol on calcium release from cultured young adult (75-day-old) mouse calvaria in the presence of indomethacin or dexamethasone was studied. Indomethacin (2.8 × 10 −7 M) or dexamethasone (10 −8 M) abolished or considerably inhibited basal calcium release. At 2.6 × 10 −7 M, 1α,25-dihydroxycholecalciferol prevented the effect of either indomethacin or dexamethasone, resulting in higher calcium release levels approximating those observed in cultures containing only 1α,25-dihydroxycholecalciferol. We have shown previously that in contrast to its effect on neonatal mouse calvaria in culture, 1α25-dihydroxycholecalciferol either failed to enhance or even inhibited basal calcium release from cultured 75-day-old mouse calvaria. Furthermore, 1α,25-dihydroxycholecalciferol inhibited PTH- or PGE 2-enhanced calcium release from such cultures. These studies demonstrated that, at the same concentration, 1α,25-dihydroxycholecalciferol decreases high calcium release due to various bone resorption-stimulating factors and increases low calcium release values due to various bone resorption-inhibiting factors. This suggested that this vitamin D 3 metabolite directly regulates the degree of bone resorption at the bone tissue level resulting in a local calcium ‘homeostasis’.