Influence of intratubular pressure on proximal tubular compliance and capillary diameter in the rat kidney

1979 ◽  
Vol 382 (2) ◽  
pp. 179-187 ◽  
Author(s):  
Peter Koch Jensen ◽  
Kenneth Steven



1983 ◽  
Vol 244 (2) ◽  
pp. E109-E114 ◽  
Author(s):  
U. Pfeifer ◽  
M. Warmuth-Metz

Adult male Sprague-Dawley rats were injected intraperitoneally with 5 U insulin/kg body wt (45 animals). As determined by quantitative electron microscopy, the volume fraction and the numerical density of autophagic vacuoles (AV) in proximal tubular cells decreased within 10 min by 46 and 26%, respectively. A partial recovery of the AV volume fraction was observed 20 and 30 min after the injection contrary to our previous findings with liver (J. Cell Biol. 78: 152-167, 1978). In an additional experiment (12 animals) it was shown that an insulin dose of 0.5 U but not of 0.05 U/kg body wt reduced the AV volume fraction to an extent similar to that of 5 U. To eliminate possible secondary effects, Ringer solution containing 0.8 microM insulin was dropped intravitally for 15 min to one pole of the decapsulated kidney and Ringer solution without additions to the other pole (8 animals). After intravital fixation, the AV volume fraction and numerical density in proximal tubular cells was found to be reduced under the influence of insulin by 22 and 36%, respectively. This data shows that insulin inhibits the process of cellular autophagy in proximal tubular cells of the kidney.



1975 ◽  
Vol 229 (3) ◽  
pp. 813-819 ◽  
Author(s):  
A Grandchamp ◽  
Scherrer ◽  
D Scholer ◽  
J Bornand

The effect of small changes in intraluminal hydrostatic pressure (P) on the tubular radius (r) and the net fluid reabsorption per unit of surface area of the tubular wall (Js) has been studied in the proximal tubule of the rat kidney. The split-drop method was used to simultaneously determine Js and r. Two standardized split-drop techniques A and B allow selective change in P. P was 31.6 +/- 1.3 mmHg in technique A and 15.5 +/- 1.5 in technique B. The pressure difference significantly affected the tubular radius; r was 21.9 +/- 0.4 and 18.6 +/- 0.5 mum in the split drop A and B, respectively. In contrast, net transepithelial fluid reabsorption Js was unchanged. Js amounted to 2.72 +/- 0.20, and 2.78 +/- 0.33 10(-5) cm3 cm-2 s-1 in split drop A and B. The absence of variations in Js could result from two opposite effects of pressure. P might enhance Js by increased ultrafiltration. However, the rise in r might decrease the density of the intraepithelial transport paths per unit area of tubular wall and therefore might decrease Js.





1980 ◽  
Vol 238 (3) ◽  
pp. F205-F209 ◽  
Author(s):  
K. M. Gaudio ◽  
N. J. Siegel ◽  
J. P. Hayslett ◽  
M. Kashgarian

To define the interrelationship between changes in total renal blood flow (TRBF) and proximal tubular hydrostatic pressure (PTP), rats were studied 2, 3, 4, 6, 12, 18, and 24 h after bilateral ureteral occlusion (BUO). In control animals, a peak rise in both TRBF (3.52 +/- 0.26 ml . min-1 . 100 g body wt-1 . kidney-1) and PTP (28.6 +/- 1.3 mmHg) occurred 3 h after BUO. At each subsequent time interval, both TRBF and PTP fell, so that by 24 h after BUO, TRBF was 1.53 +/- 0.34 and PTP was 16.5 +/- 0.6, while in sham-operated rats the values were 2.52 +/- 0.22 ml . min-1 . g body wt-1 . kidney-1 and 12.8 +/- 0.2 mmHg, respectively. In animals treated with indomethacin (10 mg/kg) at the time of BUO, the alterations in both TRBF and PTP were completely ameliorated. At 3 h, TRBF was 1.8 +/- 0.32 ml . min-1 . 100 g body wt-1 . kidney-1 and PTP was 15.3 +/- 1.0 mmHg. TRBF and PTP remained essentially unchanged at each subsequent time period. These data indicate that 1) alterations in TRBF and PTP follow a similar and parallel pattern during BUO; 2) the pattern of changes in TRBF and PTP can be eliminated by treatment with indomethacin; and 3) renal hemodynamics appear to be the dominant factor in producing these changes during the first 12 h after BUO, whereas a sustained increase in tubular hydrostatic pressure may play a primary role in decreasing TRBF 12-24 h after ureteral occlusion.



1981 ◽  
Vol 241 (3) ◽  
pp. F238-F243
Author(s):  
D. A. Hartupee ◽  
A. H. Gillies ◽  
F. G. Knox

Previous studies concerning the measurement of single nephron filtration rate have shown that collections of proximal tubular fluid, in which an oil drop is held in a constant position, do not affect intratubular pressure in the early proximal tubule in the hydropenic rat. Since intratubular pressures are higher in the dog than the rat, we investigated the effect of position-controlled collections on proximal pressure and single nephron filtration rate (SNGFR) in the dog. During position-controlled collections, early proximal pressure fell 5.8 +/- 0.9 mmHg and SNGFR was 76.3 +/- 5.3 nl/min. During proximal re-collections, in which proximal pressure was maintained near the free-flow value using a long immobile oil block, SNGFR was significantly less, 44.4 +/- 5.5 nl/min. For each micropunctured kidney, SNGFR was also estimated by dividing GFR by the number of glomeruli (mean, 5.4 +/- 0.5 X 10(5)). Estimated SNGFR (50.9 +/- 6.3 nl/min) was not significantly different from pressure-controlled SNGFR but was significantly less than position-controlled SNGFR. Accordingly, in the dog, early proximal pressure decreases during position-controlled collection of proximal tubular fluid, resulting in an overestimation of SNGFR. This artifact can be avoided by controlling the intratubular pressure during collection of tubular fluid.



2020 ◽  
Vol 21 (4) ◽  
pp. 1473
Author(s):  
Sang Heon Suh ◽  
Hong Sang Choi ◽  
Chang Seong Kim ◽  
In Jin Kim ◽  
Hyunju Cha ◽  
...  

Histone deacetylases have been a target of therapy for organ fibrosis. Here, we report the protective effect of CG200745 (CG), a novel histone deacetylase inhibitor, on tubulointerstitial fibrosis in Col4a3−/− mice, a murine model of Alport syndrome. Morphological analyses revealed CG treatment markedly alleviated kidney fibrosis in Col4a3−/− mice at the age of 7 weeks. CG prevented the activation of transforming growth factor β (TGFβ) and its downstream SMAD signaling in the kidney of Col4a3−/− mice. As critical upstream regulators of TGFβ signaling, immunoblotting of whole kidney lysate of Col4a3−/− mice reveled that intra-renal renin–angiotensin system (RAS) was activated with concurrent upregulation of inflammation and apoptosis, which were effectively suppressed by CG treatment. CG suppressed both activation of RAS and up-regulation of TGFβ signals in angiotensin II-stimulated HK-2 cells, a human kidney proximal tubular epithelial cell line. CG inhibited activation of TGFβ-driven signals and fibrosis in NRK-49F cells, a rat kidney fibroblast cell line, under angiotensin II-rich conditions. Collectively, CG was found to be effective both in proximal tubular epithelial cells by inhibiting local RAS and TGFβ signaling activation, as well as in fibroblasts by blocking their transition to myofibroblasts, attenuating renal fibrosis in a murine model of Alport syndrome.





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