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首页> 外文期刊>American Journal of Physiology >Reduced expression of renal Na+ transporters in rats with PTH-induced hypercalcemia.
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Reduced expression of renal Na+ transporters in rats with PTH-induced hypercalcemia.

机译：PTH诱导的高钙血症大鼠肾Na +转运蛋白表达降低。

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The purpose of this study was to evaluate whether the natriuresis and polyuria seen in parathyroid hormone (PTH)-induced hypercalcemia are associated with dysregulation of renal Na transporters. Rats were infused with three different doses of human PTH [PTH (1-34); 7.5, 10, and 15 microg.kg(-1).day(-1) s.c.] or vehicle for 48 h using osmotic minipumps. The rats treated with PTH developed significant hypercalcemia (plasma total calcium levels: 2.71 +/- 0.03, 2.77 +/- 0.02, and 3.42 +/- 0.06 mmol/l, respectively, P < 0.05 compared with corresponding controls). The rats with severe hypercalcemia induced by high-dose PTH developed a decreased glomerular filtration rate (GFR), increased urine output, reduced urinary osmolality, increased urinary Na excretion, and fractional excretion of Na. This was associated with downregulation (calculated as a fraction of control levels) of whole kidney expression of type 2 Na-P(i) cotransporter (NaPi-2; 16 +/- 6%), type 3 Na/H exchanger (NHE3; 42 +/- 7%), Na-K-ATPase (55 +/- 2%), and bumetanide-sensitive Na-K-2Cl cotransporter (BSC-1; 25 +/- 4%). In contrast, an upregulation of the Ca(2+)-sensing receptor (CaR) was observed. Rats treated with moderate-dose PTH exhibited unchanged GFR but decreased urinary concentration. The whole kidney expression of NHE3 (52 +/- 8%) and NaPi-2 (26 +/- 5%) was persistently decreased, whereas BSC-1 and Na-K-ATPase protein levels were not altered. CaR expression was also increased. Moreover, rats treated with low-dose PTH showed very mild hypercalcemia but unchanged GFR, normal urinary concentration, and unchanged expression of Na transporters and CaR. In conclusion, the reduced expression of major renal Na transporters is likely to play a role in the increased urinary Na excretion and decreased urinary concentration in rats with PTH-induced hypercalcemia. Moreover, the increase in the CaR in the thick ascending limb (TAL) may indicate a potential role of the CaR in inhibiting Na transport in the TAL.
机译：这项研究的目的是评估甲状旁腺激素（PTH）引起的高钙血症中的利尿和多尿症是否与肾钠转运蛋白的失调有关。给大鼠注入三种不同剂量的人PTH [PTH（1-34）; 7.5、10和15 microg.kg（-1）.day（-1）s.c.]或媒介物使用渗透性微型泵持续48小时。用PTH治疗的大鼠发生了明显的高钙血症（血浆总钙水平分别为2.71 +/- 0.03、2.77 +/- 0.02和3.42 +/- 0.06 mmol / l，与相应对照组相比，P <0.05）。高剂量PTH引起的严重高钙血症大鼠的肾小球滤过率（GFR）降低，尿量增加，尿渗透压降低，尿钠排泄增加和钠的部分排泄。这与2型Na-P（i）共转运蛋白（NaPi-2; 16 +/- 6％），3型Na / H交换子（NHE3; 2）的全肾表达的下调（计算为对照水平的一部分）有关。 42 +/- 7％），Na-K-ATPase（55 +/- 2％）和布美他尼敏感的Na-K-2Cl共转运蛋白（BSC-1; 25 +/- 4％）。相反，观察到Ca（2+）感应受体（CaR）的上调。用中剂量PTH治疗的大鼠表现出不变的GFR，但尿液浓度降低。 NHE3（52 +/- 8％）和NaPi-2（26 +/- 5％）的整个肾脏表达持续降低，而BSC-1和Na-K-ATPase蛋白水平没有改变。 CaR表达也增加。此外，用小剂量PTH治疗的大鼠表现出非常轻度的高钙血症，但GFR不变，尿液浓度正常，Na转运蛋白和CaR的表达不变。总之，在PTH引起的高钙血症大鼠中，主要肾脏Na转运蛋白表达的降低可能在尿Na排泄增加和尿液浓度降低中起作用。此外，厚上升肢（TAL）中CaR的增加可能表明CaR抑制TAL中Na转运的潜在作用。

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