胞外Ca2 + 通过激活甲状旁腺细胞表面的钙敏感受体 (CaR) ,可独立、快速地调节甲状旁腺激素 (PTH)的释放 ,慢性肾衰继发甲旁亢 (SHPT)时 ,甲状旁腺CaR的表达减少 ,是引起甲状旁腺细胞过度分泌PTH的直接原因之一。新问世的CaR激动剂 ,可模仿甚至增强胞外Ca2 + 对CaR的作用 ,初步研究证实 ,它能降低SHPT患者血PTH水平 ,动物实验还发现它有改善骨骼病变的作用 ,因此具有良好的应用前景。 Extracellular Ca2 + regulates the release of parathyroid hormone (PTH) independently and rapidly by activating CaR on the surface of parathyroid cells. When paracrine hyperparathyroidism (SHPT) occurs in chronic renal failure, Decreased expression of glandular CaR is one of the direct causes of PTH secretion by parathyroid cells. The newly emerged CaR agonist can mimic and even enhance the effect of extracellular Ca2 + on CaR. Preliminary studies have shown that it can reduce the blood PTH level in SHPT patients. Animal experiments have also found that it has the effect of improving bone lesions and therefore has good application prospect.