Management of disturbed calcium metabolism in uraemic patients: 3. Potential perspectives--calcimimetics.

Management of disturbed calcium metabolism in uraemic patients: 3. Potential perspectives--calcimimetics.
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尿毒症患者钙代谢紊乱的治疗:3.潜在前景——拟钙剂。

DOI:
10.1093/ndt/15.suppl_5.30
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发表时间:
2000
影响因子:
--
通讯作者:
E. Ritz
E. Ritz
中科院分区:
--
文献类型:
--
作者:
M. Schömig;E. Ritz

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1993年,Brown等人从牛甲状旁腺功能障碍中克隆并鉴定了一种由功能获得性突变引起的低钙感应受体蛋白。甲状腺腺体。在尿毒症大鼠的甲状旁腺增生中,表达代谢受体与钙受体的8个跨膜连接减少,这是与甲状旁腺增生[3]相关的片段,对钙具有显著的低亲和力。与通常的纳摩尔浓度或更低浓度的甲状旁腺细胞相比,是否(毫摩尔浓度的配体受体减少了双表型调节的表达,或者它是否是特异性的)。如此低的亲和力使该蛋白能够产生未知的尿毒症。生理范围的报告刺激了肾监测对该受体内钙浓度变化的兴趣。目前尚不清楚Nemeth等人是否认为低分子量的comcalcium受体受1,25 -二羟基磅(所谓的钙化剂)和选择性维生素D的有效调节
In 1993, Brown et al.[1] cloned and characterized a explained by gain-of-function mutations causing hypocalcium-sensing receptor protein from bovine para-parathyroidism. thyroid glands. The receptor is a G-protein-dependent In hyperplastic parathyroids of uraemic rats, expresmetabotropic receptor with eight transmembrane sion of the calcium receptor is diminished and this is segments and has a remarkably low affinity for calcium associated with parathyroid hyperplasia [3]. Whether (millimolar concentrations of receptors for ligands diminishedexpressionisduetophenotypicmodulation compared with usually nanomolar or lower concentra-of the parathyroid cell or whether it is specific to the tions). Such a low affinity enables the protein to stateofuraemiaisunknown. Theinterestofnephrologmonitor changes of calcium concentrations within the ists in this receptor was stimulated by the report of physiological range. It is currently unclear whether the Nemeth et al.[4] that low molecular weight comcalcium receptor is regulated by 1, 25-dihydroxy-pounds, so-called calcimimetics, potently and selectvitamin D