Bank N, Aynedjian H S
J Clin Invest. 1975 May;55(5):994-1002. doi: 10.1172/JCI108029.
The mechanism of sodium retention by the kidney in rats with ligation of the common bile duct was studied with micropuncture techniques. 10-14 days after bile duct ligation, rats showed positive sodium balance and ascites formation. Measurements of renal blood flow and glomerular filtration rate yielded values that were not different from those in normal control animals. Likewise, single nephron filtration rte of surface nephrons was the same in the experimental rats as in the controls. Sodium reabsorption, however, was markedly increased in the proximal convoluted tubule, as well as in segments beyond the proximal convolutions. Single nephron filtration fraction, calculated from measurements of efferent arteriolar and arterial hematocrits, was significantly elevated in the cortical nephrons, even though whole kidney filtration fraction was the same as in normal rats. The calculated protein concentration of cortical peritubular blood was higher in the bile duct-ligated rats than in the normal controls. The observations are consistent with the view that sodium retention is the result of enhanced reabsorption primarily by cortical nephrons. The enhanced reabsorption can be accounted for by relative cortical ischemia due to efferent arteriolar vasoconstriction with the consequent elevation of peritubular colloid oncotic pressure.
采用微穿刺技术研究了胆总管结扎大鼠肾脏的钠潴留机制。胆总管结扎10 - 14天后，大鼠出现钠正平衡和腹水形成。肾血流量和肾小球滤过率的测量结果与正常对照动物无差异。同样，实验大鼠表层肾单位的单肾单位滤过率与对照组相同。然而，近端曲管以及近端曲管以外节段的钠重吸收明显增加。根据出球小动脉和动脉血细胞比容测量计算出的皮质肾单位单肾单位滤过分数显著升高，尽管全肾滤过分数与正常大鼠相同。胆总管结扎大鼠皮质肾小管周围血液的计算蛋白浓度高于正常对照组。这些观察结果与以下观点一致，即钠潴留主要是皮质肾单位重吸收增强的结果。重吸收增强可归因于出球小动脉血管收缩导致的相对皮质缺血，进而引起肾小管周围胶体渗透压升高。
