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首页> 外文期刊>American Journal of Physiology >Effects of a high-sodium/low-potassium diet on renal calcium, magnesium, and phosphate handling
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Effects of a high-sodium/low-potassium diet on renal calcium, magnesium, and phosphate handling

机译：高钠/低钾饮食对肾钙，镁和磷酸盐处理的影响

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摘要

The distal convoluted tubule (DCT) of the kidney plays an important role in blood pressure regulation by modulating Na+ reabsorption via the Na+-Cl~- cotrans-porter (NCC). A diet containing high salt (NaCl) and low K+ activates NCC, thereby causing Na+ retention and a rise in blood pressure. Since high blood pressure, hypertension, is associated with changes in serum calcium (Ca~(2+)) and magnesium (Mg~(2+)) levels, we hypothesized that dietary Na+ and K+ intake affects Ca~(2+) and Mg~(2+) transport in the DCT. Therefore, the present study aimed to investigate the effect of a high-Na+/1ow-K+ diet on renal Ca~(2+) and Mg~(2+) handling. Mice were divided in four groups and fed a normal-Na+/ normal-K+, normal-Na+/low-K+, high-Na+/norma!-K+, or high-Na+/low-K+ diet for 4 days. Serum and urine were collected for electrolyte and hormone analysis. Gene and protein expression of electrolyte transporters were assessed in kidney and intestine by qPCR and immunoblotting. Whereas Mg~(2+) homeostasis was not affected, the mice had elevated urinary Ca~(2+) and phosphate (Pi) excretion upon high Na+ intake, as well as significantly lower serum Ca~(2+) levels in the high-Na+/low-K+ group. Alterations in the gene and protein expression of players involved in Ca~(2+) and P_i, transport indicate that reabsorption in the proximal tubular and TAL is affected, while inducing a compensatory response in the DCT. These effects may contribute to the negative health impact of a high-salt diet, including kidney stone formation, chronic kidney disease, and loss of bone mineral density.
机译：通过Na + -Cl〜 - Cotrans-porter（NCC）调节Na + Reabling，肾脏的远端卷积小管（DCT）在血压调节中起重要作用。含有高盐（NaCl）和低k +的饮食活化NCC，从而导致Na +保持和血压升高。由于高血压高血压与血清钙（Ca〜（2+））和镁（Mg〜（2+））水平的变化有关，我们假设膳食Na +和K +摄入量影响Ca〜（2+）和Mg〜（2+）在DCT中运输。因此，本研究旨在研究高Na + / 1W-K +饮食对肾Ca〜（2+）和Mg〜（2+）处理的影响。小鼠分为四组，并喂养正常-Na + /普通-K +，正常-NA + /低k +，高Na + / norma！-K +，或高Na + / Low-K +饮食4天。收集血清和尿液，用于电解质和激素分析。通过QPCR和免疫印迹，在肾脏和肠中评估电解质转运蛋白的基因和蛋白质表达。虽然Mg〜（2+）稳态没有受到影响，但小鼠在高Na +摄入量下尿Ca〜（2+）和磷酸盐（PI）排泄，以及显着降低高分子的血清Ca〜（2+）水平-NA + /低K +组。参与Ca〜（2+）和P_I的球员基因和蛋白表达的改变，转运表明近端管状和缩略的重吸收受影响，同时在DCT中诱导补偿响应。这些效果可能有助于高盐饮食的负面健康影响，包括肾结石形成，慢性肾病和骨密度损失。

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