甲状旁腺激素对肾小管钙和磷酸盐处理的影响

IF 5.6 2区 医学 Q1 PHYSIOLOGY
R. Todd Alexander, Henrik Dimke
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引用次数: 5

摘要

维持钙稳态的核心是沿肾元调节钙的重吸收。为此,甲状旁腺释放甲状旁腺激素(PTH)以响应血浆钙水平的降低。这种激素通过沿肾元的PTH - 1受体起作用,增加尿中磷酸盐的排泄,减少尿中钙的排泄。在近端小管中,甲状旁腺素通过减少根尖膜中磷酸钠共转运蛋白的丰度来抑制磷酸盐的再吸收。甲状旁腺激素可能通过减少钠的重吸收来减少近端小管的钙重吸收,钠的重吸收是钙在这一节段的细胞旁运动所必需的。在厚升肢(TAL)中,甲状旁腺素增加钙的通透性,并可能增加电驱动力,从而增加TAL中钙的重吸收。最后,在远端卷积中,PTH通过增加顶端表达的钙通道TRPV5的活性和丰度来增加跨细胞钙重吸收。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effects of parathyroid hormone on renal tubular calcium and phosphate handling

Central to the maintenance of calcium homeostasis is the regulated reabsorption of calcium along the nephron. To this end, parathyroid hormone (PTH) is released from the parathyroid gland in response to lowered plasma calcium levels. This hormone acts through the PTH 1 receptor along the nephron to increase urinary phosphate excretion and decrease urinary calcium excretion. In the proximal tubule, PTH inhibits phosphate reabsorption by reducing the abundance of sodium phosphate cotransporters in the apical membrane. PTH likely decreases calcium reabsorption from the proximal tubule, by reducing the reabsorption of sodium, an event necessary for the paracellular movement of calcium across this segment. In the thick ascending limb (TAL), PTH increases calcium permeability and may increase the electrical driving force thereby increasing calcium reabsorption in the TAL. Finally, in the distal convolution, PTH acts to increase transcellular calcium reabsorption by increasing the activity and abundance of the apically expressed calcium channel TRPV5.

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来源期刊
Acta Physiologica
Acta Physiologica 医学-生理学
CiteScore
11.80
自引率
15.90%
发文量
182
审稿时长
4-8 weeks
期刊介绍: Acta Physiologica is an important forum for the publication of high quality original research in physiology and related areas by authors from all over the world. Acta Physiologica is a leading journal in human/translational physiology while promoting all aspects of the science of physiology. The journal publishes full length original articles on important new observations as well as reviews and commentaries.
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