Effect of medullary tonicity on urinary sodium excretion in the rat.
Effect of medullary tonicity on urinary sodium excretion in the rat.
复制标题
髓质张力对大鼠尿钠排泄的影响。
DOI：
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发表时间：
1982
影响因子：
15.9
通讯作者：
R. Parma
中科院分区：
文献类型：
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作者：
H. Reineck;R. Parma
在本实验室以前的报告中，我们已经提出，延髓张力的降低减少了Henle钠重吸收的细上升环，并部分负责伴随10%体重林格氏负荷的尿钠排泄的幅度。根据这一假设，人们会认为与水利尿相关的髓质冲洗也会导致尿钠排泄，但这并没有发生。然而，可能需要增加近端小管的递送来证明髓质张力对尿钠排泄的影响。设计了微穿刺研究，通过在有和没有降低骨髓张力的动物中增加2%林格氏负荷的远端输送来测试这种可能性。在最初的一系列实验中，α-肾上腺素能激动剂可乐定用于诱导水利尿。当单独给药时，该药物引起尿渗透压明显降低和尿流速增加，但对浅表或髓质肾单位的近端重吸收没有影响，也不改变尿钠排泄。用2%体重的林格氏溶液进行容量扩张导致近端重吸收显著下降，钠排泄轻微增加。当给予进行水利尿的动物相同程度的体积扩张时，绝对和分数钠排泄显著增加。在第二组研究中，仅通过在微穿刺前1小时切除左输尿管，左肾髓质张力降低。当这些动物输注2%体重的林格氏溶液时，近端重吸收减少，仅从左肾观察到钠排泄显著增加。最后，评价了在2%林格氏液负荷期间，水利尿对浅表肾单位早期和晚期远端小管钠输送分数的影响。在单独2%林格氏负荷和2%林格氏负荷加水利尿期间，这两个部位的输注量相当。从这些数据中，我们得出结论，髓质张力确实影响肾钠处理，但这种影响只在近端重吸收减少的条件下才表现在最终尿液中。这些数据还表明，这种影响仅限于延髓肾单位，可能是本地化的薄的Henle袢升支。
In previous reports from this laboratory we have suggested that a reduction in medullary tonicity decreases the thin ascending loop of Henle sodium reabsorption and is in part responsible for the magnitude for the natriuresis accompanying 10% body weight Ringer loading. According to this postulate, one would expect that the medullary washout associated with water diuresis would also result in a natriuresis, but this does not occur. It is possible, however, that increased delivery from the proximal tubule is necessary to demonstrate an effect of medullary tonicity on urinary sodium excretion. Micropuncture studies were designed to test that possibility by increasing distal delivery by 2% Ringer loading in animals with and without reduced medullary tonicity. In an initial series of experiments the alpha-adrenergic agonist clonidine was used to induce a water diuresis. When given alone, this agent caused a marked decrease in urine osmolality and an increase in urine flow rate but had no effect on proximal reabsorption in either superficial or juxtamedullary nephrons, and did not alter urinary sodium excretion. Volume expansion with 2% body weight Ringer solution resulted in a significant fall in proximal reabsorption and a trivial increment in sodium excretion. When this same degree of volume expansion was conferred on animals undergoing a water diuresis, a marked increase in absolute and fractional sodium excretion occurred. In a second group of studies medullary tonicity was reduced in the left kidney only by removal of the left ureter 1 h before micropuncture. When these animals were infused with 2% body weight Ringer solution, proximal reabsorption was decreased in juxtamedullary nephrons, and a marked increase in sodium excretion was observed only from the left kidney. Finally, the effect of water diuresis on fractional sodium delivery to the early and late distal tubule of superficial nephrons during 2% Ringer loading was evaluated. Delivery to both of these sites was comparable after 2% Ringer loading alone and during 2% Ringer loading plus water diuresis. From these data, we conclude that medullary tonicity does influence renal sodium handling but that this effect is manifest in the final urine only under conditions in which proximal reabsorption is decreased. The data also suggest that this effect is limited to juxtamedullary nephrons and is probably localized to the thin ascending limb of the loop of Henle.