MICROPUNCTURE STUDY OF RENAL PHOSPHATE TRANSPORT IN RATS WITH CHRONIC RENAL-FAILURE AND SECONDARY HYPER-PARATHYROIDISM
MICROPUNCTURE STUDY OF RENAL PHOSPHATE TRANSPORT IN RATS WITH CHRONIC RENAL-FAILURE AND SECONDARY HYPER-PARATHYROIDISM
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DOI：
10.1172/jci109014
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发表时间：
1978-01-01
影响因子：
15.9
通讯作者：
AYNEDJIAN, HS
中科院分区：
文献类型：
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作者：
BANK, N;SU, WS;AYNEDJIAN, HS
在大鼠中进行了显微穿刺研究，以确定慢性肾衰竭和继发性甲状旁腺功能亢进中磷酸盐肾小管转运的变化。大鼠行肾大部切除术（NX），低钙高磷饲料喂养3-4 wk。其他组包括正常对照动物、输注磷酸钠以提高磷酸盐滤过负荷的正常大鼠、实验当天次全切除甲状旁腺（PTX）的NX大鼠和输注磷酸钠的正常PTX大鼠。在次全NX大鼠中，由于单个肾单位滤过率高，滤过磷酸盐/肾单位显著增加，近端小管液血浆磷酸盐比值> 1.0，近端小管中磷酸盐重吸收分数降低。最终尿液中磷酸盐含量高于远曲小管表面。次全NX大鼠的急性PTX导致近端磷酸盐重吸收显著增加，尿磷酸盐变得约等于表面远端小管中剩余的磷酸盐。正常大鼠的磷酸盐负荷减少了近端小管的重吸收分数，但尿磷酸盐并不大于表面远端小管末端的磷酸盐。正常磷酸盐负荷动物的急性PTX对近端肾小管磷酸盐重吸收没有显著影响。这些观察结果表明，磷酸盐稳态在慢性肾功能衰竭是通过抑制近端磷酸盐重吸收，抵消了大大增强的内在能力的重吸收。此外，大量的尿磷酸盐与集合管的分泌或深肾单位的不成比例的高贡献是一致的。磷酸盐转运的变化是由甲状旁腺激素介导的，并且通过急性去除该激素而完全消除。
Micropuncture studies were carried out in rats to determine changes in tubular transport of phosphate which occur in chronic renal failure and secondary hyperparathyroidism. Rats underwent subtotal nephrectomy (NX) and were fed a low Ca high P diet for 3-4 wk. Other groups consisted of normal control animals, normal rats infused with sodium phosphate to raise filtered load of phosphate, subtotal NX rats parathyroidectomized (PTX) on the day of experiment, and normal PTX rats infused with sodium phosphate. Filtered phosphate/nephron is markedly increased in subtotal NX rats due to high single nephron filtration rates, proximal tubular fluid plasma phosphate ratios are > 1.0 and fractional reabsorption of phosphate is decreased in the proximal tubule. More phosphate was present in the final urine than in surface distal convoluted tubules. Acute PTX in subtotal NX rats resulted in a striking increase in proximal phosphate reabsorption, and urinary phosphate became approximately equal to that remaining in surface distal tubules. Phosphate loading in normal rats reduced fractional reabsorption in the proximal tubule, but urinary phosphate was not greater than that at the end of surface distal tubules. Acute PTX in normal phosphate-loaded animals had no significant effect on proximal tubular phosphate reabsorption. These observations suggest that phosphate homeostasis in chronic renal failure is achieved by inhibition of proximal phosphate reabsorption, counteracting a greatly enhanced intrinsic capacity for reabsorption. In addition, the large amount of urinary phosphate is consistent either with secretion by the collecting ducts or with a disproportionately high contribution by deep nephrons. The changes in phosphate transport are mediated by parathyroid hormone and are completely abolished by acute removal of the hormone.