Gordeladze J O, Gautvik K M
Biochem Pharmacol. 1986 Mar 15;35(6):899-902. doi: 10.1016/0006-2952(86)90074-2.
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.
在大鼠骨细胞的微粒体部分中，而非肾细胞的微粒体部分，24,25-二羟维生素D3（24,25-(OH)2 D3）以剂量依赖性方式（1 nM及以上）抑制甲状旁腺激素（PTH）激活的腺苷酸环化酶。相反，24,25-(OH)2D3增强骨中降钙素（CT）刺激的环化酶活性，但减弱肾中CT诱导的环化酶反应。在超正常浓度下，1,25-二羟维生素D3（1,25-(OH)2D3）也能够降低骨中PTH刺激的腺苷酸环化酶活性。相比之下，这两种维生素D3代谢物均不干扰促甲状腺素释放激素（TRH）或血管活性肠肽（VIP）对垂体细胞膜腺苷酸环化酶的刺激。这些发现对于预防PTH过度作用和骨质脱矿可能具有重要的治疗意义。
