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本文引用的文献

1
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2
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J Clin Invest. 1964 Oct;43(10):1928-37. doi: 10.1172/JCI105067.
3
[A simple colorimetric method of inulin determination in renal clearance studies on metabolically normal subjects and diabetics].[一种用于代谢正常受试者和糖尿病患者肾脏清除率研究中菊粉测定的简单比色法]
Klin Wochenschr. 1955 Aug 1;33(29-30):729-30. doi: 10.1007/BF01473295.
4
Role of medullary hemodynamics in the natriuresis of drug-induced renal vasodilation in the rat.髓质血流动力学在大鼠药物诱导的肾血管舒张所致利钠中的作用
Circ Res. 1980 Dec;47(6):839-44. doi: 10.1161/01.res.47.6.839.
5
Nephron heterogeneity in renal excretion of sodium and potassium in the rat.大鼠肾脏钠和钾排泄中的肾单位异质性
Am J Physiol. 1980 Aug;239(2):F187-93. doi: 10.1152/ajprenal.1980.239.2.F187.
6
Effects of alterations in urine flow rate on prostaglandin E excretion in conscious dogs.尿流率改变对清醒犬前列腺素E排泄的影响。
Am J Physiol. 1980 Feb;238(2):F107-11. doi: 10.1152/ajprenal.1980.238.2.F107.
7
Relationship between extracellular volume and fluid reabsorption by the rat nephron.大鼠肾单位细胞外液量与液体重吸收之间的关系。
Am J Physiol. 1969 Jul;217(1):6-12. doi: 10.1152/ajplegacy.1969.217.1.6.
8
Depression of fractional sodium reabsorption by the proximal tubule of the dog without sodium diuresis.犬近端小管对钠的重吸收分数降低,无钠利尿。
J Clin Invest. 1968 Jul;47(7):1561-72. doi: 10.1172/JCI105848.
9
Natrriuresis produced by vasopressin or hemorrhage during water diuresis in the dog.犬在水利尿期间由血管加压素或出血引起的利钠作用。
Am J Physiol. 1970 Sep;219(3):658-65. doi: 10.1152/ajplegacy.1970.219.3.658.
10
Evidence for urinary dilution by the collecting tubule.集合管对尿液稀释的证据。
Am J Physiol. 1972 Oct;223(4):898-902. doi: 10.1152/ajplegacy.1972.223.4.898.

髓质张力对大鼠尿钠排泄的影响。

Effect of medullary tonicity on urinary sodium excretion in the rat.

作者信息

Reineck H J, Parma R

出版信息

J Clin Invest. 1982 Apr;69(4):971-8. doi: 10.1172/jci110536.

DOI:10.1172/jci110536
PMID:7076854
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC370151/
Abstract

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.

摘要

在本实验室之前的报告中,我们曾提出髓质张力降低会减少亨氏袢升支细段对钠的重吸收,并且在一定程度上导致了伴随10%体重的林格液负荷所出现的利钠现象。根据这一假设,人们可能会预期与水利尿相关的髓质冲洗也会导致利钠,但实际并非如此。然而,有可能需要近端小管增加输送量才能显示髓质张力对尿钠排泄的影响。微穿刺研究旨在通过在髓质张力降低和未降低的动物中给予2%的林格液负荷来增加远端输送量,从而验证这一可能性。在最初的一系列实验中,使用α-肾上腺素能激动剂可乐定诱导水利尿。单独给予该药物时,会导致尿渗透压显著降低和尿流率增加,但对浅表肾单位和近髓肾单位的近端重吸收均无影响,也不会改变尿钠排泄。给予2%体重的林格液进行容量扩张会导致近端重吸收显著下降,钠排泄略有增加。当对处于水利尿状态的动物给予相同程度的容量扩张时,绝对和分数钠排泄均显著增加。在第二组研究中,仅通过在微穿刺前1小时切除左输尿管来降低左肾的髓质张力。当给这些动物输注2%体重的林格液时,近髓肾单位的近端重吸收降低,仅左肾观察到钠排泄显著增加。最后,评估了在2%林格液负荷期间水利尿对浅表肾单位早期和晚期远端小管分数钠输送的影响。单独给予2%林格液负荷后以及2%林格液负荷加水利尿期间,输送到这两个部位的情况相当。根据这些数据,我们得出结论,髓质张力确实会影响肾脏对钠的处理,但这种影响仅在近端重吸收降低的情况下才会在终尿中表现出来。数据还表明,这种影响仅限于近髓肾单位,可能定位于亨氏袢升支细段。