Regulation of proximal tubular fluid reabsorption in the rat kidney

1985 ◽  
Vol 405 (S1) ◽  
pp. S131-S135 ◽  
Author(s):  
D. A. H�berle ◽  
J. M. Davis
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.


1984 ◽  
Vol 247 (1) ◽  
pp. F151-F157 ◽  
Author(s):  
S. W. Weinstein ◽  
R. Klose ◽  
J. Szyjewicz

The majority of the oxygen consumed by the rat kidney appears to occur in the proximal tubule. Therefore changes in metabolically linked ion transport in this segment of the nephron should result in changes in renal oxygen consumption. To study the role of bicarbonate reabsorption in metabolically linked proximal tubular ion transport a series of micropuncture-clearance-extraction experiments were performed comparing the effects of the carbonic anhydrase inhibitor benzolamide and of hypertonic sodium bicarbonate infusion with control conditions in the rat. End-proximal tubular fluid and chloride reabsorption were measured. From these, the rates of sodium and bicarbonate reabsorption were estimated. Simultaneously with the tubular fluids, extraction collections were obtained for determination of renal oxygen consumption. Both benzolamide and hypertonic bicarbonate reduced proximal tubular fluid reabsorption while concomitantly reducing the transepithelial gradient for chloride. The mean rate of renal oxygen consumption did not differ from the control rate in either experimental group and could be dissociated from the calculated net rates of proximal tubular sodium, chloride, and bicarbonate reabsorption. We interpret these data as evidence that proximal tubular hydrogen ion secretion supporting bicarbonate reabsorption requires at most small amounts of oxidative energy, less than detectable by these techniques. The data, in contrast, support the conclusion that the chloride-bicarbonate transepithelial gradient appears to be an important passive driving force in vivo for proximal tubular fluid reabsorption.


2005 ◽  
Vol 289 (2) ◽  
pp. R620-R626 ◽  
Author(s):  
Kay-Pong Yip

A nonobstructing optical method was developed to measure proximal tubular fluid reabsorption in rat nephron at 0.25 Hz. The effects of uncaging luminal nitric oxide (NO) on proximal tubular reabsorption were investigated with this method. Proximal fluid reabsorption rate was calculated as the difference of tubular flow measured simultaneously at two locations (0.8–1.8 mm apart) along a convoluted proximal tubule. Tubular flow was estimated on the basis of the propagating velocity of fluorescent dextran pulses in the lumen. Changes in local tubular flow induced by intratubular perfusion were detected simultaneously along the proximal tubule, indicating that local tubular flow can be monitored in multiple sites along a tubule. The estimated tubular reabsorption rate was 5.52 ± 0.38 nl·min−1·mm−1 ( n = 20). Flash photolysis of luminal caged NO (potassium nitrosylpentachlororuthenate) was induced with a 30-Hz UV nitrogen-pulsed laser. Release of NO from caged NO into the proximal tubule was confirmed by monitoring intracellular NO concentration using a cell-permeant NO-sensitive fluorescent dye (DAF-FM). Emission of DAF-FM was proportional to the number of laser pulses used for uncaging. Photolysis of luminal caged NO induced a dose-dependent inhibition of proximal tubular reabsorption without activating tubuloglomerular feedback, whereas uncaging of intracellular cGMP in the proximal tubule decreased tubular flow. Coupling of this novel method to measure reabsorption with photolysis of caged signaling molecules provides a new paradigm to study tubular reabsorption with ambient tubular flow.


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