Parathyroid hormone action on phosphate transport is inhibited by high osmolality.
Parathyroid hormone action on phosphate transport is inhibited by high osmolality.
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高渗透压会抑制甲状旁腺激素对磷酸盐转运的作用。
DOI：
10.1152/ajprenal.1990.258.5.f1336
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Murer,H
中科院分区：
文献类型：
--
作者：
Kempson,SA;Helmle,C;Abraham,MI;Murer,H
甲状旁腺激素（PTH）可快速抑制Na（+）-磷酸盐共转运，其特征为最大转运速率降低，且这种抑制作用不依赖于从头蛋白质合成。本研究确定PTH对Na（+）-磷酸盐共转运的作用是否至少部分通过质膜中Na（+）-磷酸盐共转运蛋白的快速内吞内化介导。辣根过氧化物酶，一种液相标记物，被用来证明在负鼠肾（OK）上皮细胞在单层培养中的内吞作用的存在。通过添加蔗糖将培养基渗透压摩尔浓度增加至500 mosmol/kgH 2 O，在1小时内对内吞作用产生80%的抑制。将细胞放回正常培养基后，抑制作用逆转。在正常渗透压（281 mosmol/kgH 2 O）下，用PTH（10（-8）M）孵育OK细胞单层3小时，可抑制Na（+）-磷酸盐共转运（4分钟摄取）56- 67%。在高渗性培养基（513 mosmol/kgH 2 O）中，当胞吞作用被抑制时，PTH仅抑制Na（+）-磷酸盐共转运25- 39%，这一变化与正常培养基中的抑制作用显著不同。高渗对PTH抑制Na（+）-H+交换或PTH刺激细胞内腺苷3 '，5'-环一磷酸没有影响。我们的结论是，PTH对Na（+）-磷酸盐共转运的完全抑制作用可能需要一个完整的内吞机制。
Parathyroid hormone (PTH) produces rapid inhibition of Na(+)-phosphate cotransport, characterized by a decreased maximal rate of transport, and the inhibition is independent of de novo protein synthesis. The present study determined whether the action of PTH on Na(+)-phosphate cotransport is mediated, at least in part, by rapid endocytic internalization of Na(+)-phosphate cotransporters present in the plasma membrane. Horseradish peroxidase, a fluid-phase marker, was used to demonstrate the presence of endocytosis in opossum kidney (OK) epithelial cells in monolayer culture. An increase in medium osmolality to 500 mosmol/kgH2O, by addition of sucrose, produced 80% inhibition of endocytosis within 1 h. The inhibition was reversed on returning the cells to normal medium. Incubation of OK cell monolayers with PTH (10(-8) M) for 3 h at normal osmolality (281 mosmol/kgH2O) inhibited Na(+)-phosphate cotransport (4 min uptakes) by 56-67%. In hyperosmolar medium (513 mosmol/kgH2O), when endocytosis was inhibited, PTH inhibited Na(+)-phosphate cotransport by only 25-39%, a change that was significantly different from the inhibition in normal medium. Hyperosomolality had no effect on PTH inhibition of Na(+)-H+ exchange or on PTH stimulation of intracellular adenosine 3',5'-cyclic monophosphate. We conclude that the full inhibitory action of PTH on Na(+)-phosphate cotransport may require an intact endocytic mechanism.