Ulfendahl H R, Ericson A C, Göransson A, Källskog O, Sjöquist M
Klin Wochenschr. 1982 Sep 15;60(18):1071-6. doi: 10.1007/BF01715837.
The intrinsic myogenic hypothesis and the tubuloglomerular feedback mechanism (TGF) give the presently most cherished explanation to the autoregulation of renal blood flow and glomerular filtration rate. A series of experiments was performed on young, normohydrated rats in order to evaluate the importance of TGF as an autoregulatory factor of the single nephron glomerular filtration rate (SNGFR) in superficial and juxtamedullary nephron populations. Micropuncture techniques were applied to tubular structures of the renal surface and on the papilla for the measurement of hydrostatic pressures and SNGFR. The SNGFR was also measured with a modified Hanssen technique. A TV-technique was used to record the urine free flow rate in the loop of Henle. The net driving forces for glomerular filtration at the afferent end of the glomerular capillaries were estimated to be 19 and 47 mm Hg for superficial and juxtamedullary nephrons respectively, when the urine flow at the macula densa was zero. The SNGFR of the two nephron populations amounted to 29.6 and 84.1 nl . min-1 . g-1 K.W., as measured with the micropuncture technique. With a modified Hanssen technique the corresponding values were 25.8 and 27.7 nl . min-1 . g-1 K.W. (kidney weight). The SNGFR was found to be well autoregulated when the urine flow at the macula densa was intact, but not when the urine flow was interrupted. The flow rate in the loop of Henle was in free flow conditions 7.3 nl . min-1 . g-1 K.W. which shall be compared with 19.2 nl . min-1 . g-1 K.W. when the urine flow to the macula densa was zero. We conclude that SNGFR is mainly autoregulated by the TGF-mechanism in young, normohydrated rats at lower arterial pressures. In normal conditions TGF is highly activated for juxtamedullary nephrons, but not for the superficial ones. The high urine flow rate in the loop of Henle at reduced flow rates at the macula densa may invalidate the use of loop blockade in studies of water and solute transfer across the loop walls.
肌源性假说和管球反馈机制（TGF）为肾血流量和肾小球滤过率的自身调节提供了目前最受认可的解释。为了评估TGF作为浅表肾单位和近髓肾单位群体中单个肾单位肾小球滤过率（SNGFR）自身调节因子的重要性，对年轻的、水合正常的大鼠进行了一系列实验。采用微穿刺技术对肾表面和肾乳头的肾小管结构进行测量，以测定静水压和SNGFR。SNGFR也采用改良的汉森技术进行测量。采用电视技术记录亨氏袢中的无尿流率。当致密斑处尿流为零时，浅表肾单位和近髓肾单位肾小球毛细血管传入端的肾小球滤过净驱动力估计分别为19和47 mmHg。用微穿刺技术测量，两个肾单位群体的SNGFR分别为29.6和84.1 nl·min-1·g-1 K.W.。采用改良的汉森技术，相应的值分别为25.8和{27.7} nl·min-1·g-1 K.W.（肾重）。当致密斑处尿流完整时，发现SNGFR能很好地自身调节，但当尿流中断时则不然。在自由流动条件下，亨氏袢中的流速为7.3 nl·min-1·g-1 K.W.，与致密斑处尿流为零时的19.2 nl·min-1·g-1 K.W.相比。我们得出结论，在动脉血压较低的年轻、水合正常的大鼠中，SNGFR主要由TGF机制自身调节。在正常情况下，TGF在近髓肾单位中高度激活，但在浅表肾单位中则不然。在致密斑处流速降低时，亨氏袢中高尿流率可能会使在研究水和溶质跨袢壁转运时使用袢阻断剂无效。
