Silver J, Moallem E, Epstein E, Kilav R, Naveh-Many T
Nephrology Services, Hadassah University Hospital, Jerusalem, Israel.
Curr Opin Nephrol Hypertens. 1994 Jul;3(4):379-85. doi: 10.1097/00041552-199407000-00003.
Ca2+ binds to a parathyroid cell Ca2+ receptor, which is G protein-coupled and activates inositol triphosphate production. Mutations in the Ca(2+)-sensing receptor gene cause familial hypocalciuric hypercalcemia and neonatal severe hyperparathyroidism. Chronic hypocalcemia increases parathyroid hormone messenger RNA levels and parathyroid cell hyperplasia. Parathyroid cells in vitro are heterologous in their response to Ca2+. The concept of a higher Ca2+ set-point in secondary hyperparathyroidism is controversial. Calcitriol is more effective than the less hypercalcemia analogues in decreasing parathyroid hormone messenger RNA and immunoreactive parathyroid hormone levels, and its kinetics are well established. Phosphate and estrogens regulate the parathyroid independently of 1,25 dihydroxyvitamin D3 and Ca2+. The physiology of the effects of endothelin and insulin-like growth factors on the parathyroid need to be established. Important advances are being made in understanding the regulation of parathyroid hormone synthesis and secretion, which are relevant to both normal physiology and the pathogenesis and treatment of diseases such as the secondary hyperparathyroidism of renal failure and osteoporosis.
钙离子与甲状旁腺细胞的钙离子受体结合，该受体是G蛋白偶联型的，并激活肌醇三磷酸的生成。钙离子敏感受体基因的突变会导致家族性低钙血症性高钙血症和新生儿重症甲状旁腺功能亢进。慢性低钙血症会增加甲状旁腺激素信使核糖核酸水平和甲状旁腺细胞增生。体外培养的甲状旁腺细胞对钙离子的反应具有异质性。继发性甲状旁腺功能亢进中较高钙离子设定点的概念存在争议。骨化三醇在降低甲状旁腺激素信使核糖核酸和免疫反应性甲状旁腺激素水平方面比低钙血症类似物更有效，并且其动力学已得到充分证实。磷酸盐和雌激素独立于1,25-二羟维生素D3和钙离子对甲状旁腺进行调节。内皮素和胰岛素样生长因子对甲状旁腺作用的生理学机制有待确定。在理解甲状旁腺激素合成和分泌的调节方面正在取得重要进展，这与正常生理学以及诸如肾衰竭继发性甲状旁腺功能亢进和骨质疏松症等疾病的发病机制及治疗均相关。
