Mercado A, Slatopolsky E, Klahr S
J Clin Invest. 1975 Dec;56(6):1386-95. doi: 10.1172/JCI108219.
Experiments were carried out in normal dogs to characterize the mechanisms by which sodium bicarbonate administration results in increased excretion of phosphate. Infusion of sodium bicarbonate alone increased fractional phosphate excretion from 0.8 to 29.3%. During bicarbonate administration, ionized calcium fell and mean parathyroid hormone values increased from 59.6 to 230.4 muleq/ml. In the same group of dogs, administration of sodium bicarbonate plus calcium prevented the fall in ionized calcium, and parathyroid hormone levels remained unchanged. In these dogs fractional phosphate excretion increased from 2.4 to only 4.9%. Similar results were obtained in thyroparathyroidectomized dogs receiving sodium bicarbonate. In these dogs fractional excretion of phosphate increased from 0.6 to 4.5%. Under all three experimental conditions no differences were observed in sodium or bicarbonate excretion or in urinary or plasma pH. Administration of hydrochloric acid, after phosphaturia had been induced by the infusion of bicarbonate, resulted in a decrease in plasma bicarbonate and an acid urine; however, the phosphaturia persisted even in the presence of an acid urine pH. In five thyroparathyroidectomized dogs infused with parathyroid hormone throughout, administration of identical amounts of sodium as either NaCl or NaHCO3 resulted in a similar degree of phosphaturia despite significant differences in urine pH. These experiments suggest that a rise in parathyroid hormone levels, resulting from a fall in ionized calcium, is the major mechanism by which bicarbonate administration produces phosphaturia. An increased natriuresis per nephron, as a consequence of extracellular fluid volume expansion, contributes to the phosphaturia. On the other hand, alkalinization of the urine does not play a significant role in the phosphaturia seen after bicarbonate administration.
在正常犬身上进行了实验，以确定给予碳酸氢钠导致磷酸盐排泄增加的机制。单独输注碳酸氢钠可使磷酸盐排泄分数从0.8%增加至29.3%。在给予碳酸氢钠期间，离子钙下降，甲状旁腺激素平均水平从59.6升至230.4微当量/毫升。在同一组犬中，给予碳酸氢钠加钙可防止离子钙下降，甲状旁腺激素水平保持不变。在这些犬中，磷酸盐排泄分数仅从2.4%增加至4.9%。在接受碳酸氢钠的甲状旁腺切除犬中也获得了类似结果。在这些犬中，磷酸盐排泄分数从0.6%增加至4.5%。在所有三种实验条件下，钠或碳酸氢盐排泄、尿液或血浆pH均未观察到差异。在输注碳酸氢钠诱导磷尿症后给予盐酸，导致血浆碳酸氢盐减少和尿液酸化；然而，即使尿液pH呈酸性，磷尿症仍持续存在。在五只全程输注甲状旁腺激素的甲状旁腺切除犬中，给予等量的氯化钠或碳酸氢钠形式的钠，尽管尿液pH存在显著差异，但导致的磷尿症程度相似。这些实验表明，离子钙下降导致甲状旁腺激素水平升高是给予碳酸氢盐产生磷尿症的主要机制。由于细胞外液量扩张，每个肾单位钠利尿增加有助于磷尿症。另一方面，尿液碱化在给予碳酸氢盐后出现的磷尿症中不起重要作用。
