Hydroxycholecalciferols modulate parathyroid hormone and calcitonin sensitive adenylyl cyclase in bone and kidney of rats. A possible physiological role for 24,25-dihydroxy vitamin D3.

In particulate fractions from rat bone cells, but not from kidney, 24,25-(OH)2 D3 inhibits in a dose dependent manner (1 nM and above) the parathyroid hormone (PTH)-activated adenylyl cyclase. In contrast, 24,25-(OH)2D3 enhances the calcitonin (CT) stimulated cyclase in bone, but attenuates the CT-induced cyclase response in kidney. In supranormal concentrations 1,25-(OH)2D3 is also able to reduce the PTH-stimulated adenylyl cyclase in bone. In comparison, neither vitamin D3 metabolite interferes with stimulation of adenylyl cyclase from pituitary cell membranes by thyroliberin (TRH) or vasoactive intestinal polypeptide (VIP). These findings may have important therapeutical consequences in preventing excessive PTH action and bone demineralization.