Single nephron filtration, luminal flow and tubular fluid reabsorption along the proximal convolution and the pars recta of the rat kidney as influenced by luminal pressure changes

1977 ◽  
Vol 371 (3) ◽  
pp. 235-243 ◽  
Author(s):  
Wolfgang Seiller ◽  
Karl-Heinz Gertz
Keyword(s):  
Rat Kidney ◽  
Fluid Reabsorption ◽  
Pars Recta ◽  
Single Nephron ◽  
Luminal Flow ◽  
Pressure Changes ◽  
Tubular Fluid Reabsorption ◽  
Proximal Convolution

Role of luminal hydrostatic pressure in proximal tubular fluid reabsorption in the rat

1975 ◽  
Vol 229 (3) ◽  
pp. 813-819 ◽  
Author(s):  
A Grandchamp ◽  
Scherrer ◽  
D Scholer ◽  
J Bornand
Keyword(s):  
Hydrostatic Pressure ◽  
Proximal Tubule ◽  
Pressure Difference ◽  
Unit Area ◽  
Rat Kidney ◽  
Fluid Reabsorption ◽  
Proximal Tubular ◽  
Tubular Fluid Reabsorption ◽  
Selective Change

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.

TGF-initiated vascular interactions between adjacent nephrons in the rat kidney

1990 ◽  
Vol 259 (1) ◽  
pp. F60-F64 ◽  
Author(s):  
O. Kallskog ◽  
D. J. Marsh
Keyword(s):  
Radial Artery ◽  
Rat Kidney ◽  
Ringer Solution ◽  
Systemic Arterial Pressure ◽  
Tubuloglomerular Feedback ◽  
Lumbar Artery ◽  
Single Nephron ◽  
Flow Pressure ◽  
Pressure Changes ◽  
Stop Flow

We sought to determine whether tubuloglomerular feedback (TGF), activated from one nephron, affects other arterioles derived from the same cortical radial artery. Surface nephrons supplied by a single cortical radial artery were identified by injecting Ringer solution containing Fast Green from a narrow-gauge polyethylene catheter inserted via a lumbar artery into a renal artery. Stop-flow pressure was measured in an identified nephron from such a grouping. In one series, increasing end-proximal flow rate from 0 to 50 nl/min of synthetic tubular fluid in one member of an identified pair of nephrons reduced stop-flow pressure by 1.3 +/- 0.2 mmHg in the other member. When the nephrons were derived from different cortical radial arteries, the stop-flow pressure changed -0.2 +/- 0.1 mmHg. In another series, increasing flow in the adjacent nephron from 0 to 50 nl/min decreased stop-flow pressure 3.9 +/- 0.9 mmHg, and increasing flow in the adjacent nephron by the same amount when flow in the first nephron was 50 nl/min decreased stop-flow pressure 3.4 +/- 0.7 mmHg. These results indicate the operation of an interaction among nephrons derived from a common cortical radial artery. Such an interaction could produce a cooperative effect larger than that predicted from measured single-nephron responses when systemic arterial pressure changes.

Proximal tubular Na, Cl, and HCO3 reabsorption and renal oxygen consumption

1984 ◽  
Vol 247 (1) ◽  
pp. F151-F157 ◽  
Author(s):  
S. W. Weinstein ◽  
R. Klose ◽  
J. Szyjewicz
Keyword(s):  
Oxygen Consumption ◽  
Ion Transport ◽  
Rat Kidney ◽  
Fluid Reabsorption ◽  
Bicarbonate Reabsorption ◽  
Renal Oxygen Consumption ◽  
Proximal Tubular ◽  
Tubular Fluid Reabsorption ◽  
Renal Oxygen

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.

scholarly journals A computational model for simulating solute transport and oxygen consumption along the nephrons

2016 ◽  
Vol 311 (6) ◽  
pp. F1378-F1390 ◽  
Author(s):  
Anita T. Layton ◽  
Volker Vallon ◽  
Aurélie Edwards
Keyword(s):  
Oxygen Consumption ◽  
Computational Model ◽  
Solute Transport ◽  
Rat Kidney ◽  
Transport Processes ◽  
Proximal Tubules ◽  
Thick Ascending Limb ◽  
Nephron Segments ◽  
Single Nephron ◽  
Luminal Flow

The goal of this study was to investigate water and solute transport, with a focus on sodium transport (TNa) and metabolism along individual nephron segments under differing physiological and pathophysiological conditions. To accomplish this goal, we developed a computational model of solute transport and oxygen consumption (QO2) along different nephron populations of a rat kidney. The model represents detailed epithelial and paracellular transport processes along both the superficial and juxtamedullary nephrons, with the loop of Henle of each model nephron extending to differing depths of the inner medulla. We used the model to assess how changes in TNa may alter QO2 in different nephron segments and how shifting the TNa sites alters overall kidney QO2. Under baseline conditions, the model predicted a whole kidney TNa/QO2, which denotes the number of moles of Na+ reabsorbed per moles of O2 consumed, of ∼15, with TNa efficiency predicted to be significantly greater in cortical nephron segments than in medullary segments. The TNa/QO2 ratio was generally similar among the superficial and juxtamedullary nephron segments, except for the proximal tubule, where TNa/QO2 was ∼20% higher in superficial nephrons, due to the larger luminal flow along the juxtamedullary proximal tubules and the resulting higher, flow-induced transcellular transport. Moreover, the model predicted that an increase in single-nephron glomerular filtration rate does not significantly affect TNa/QO2 in the proximal tubules but generally increases TNa/QO2 along downstream segments. The latter result can be attributed to the generally higher luminal [Na+], which raises paracellular TNa. Consequently, vulnerable medullary segments, such as the S3 segment and medullary thick ascending limb, may be relatively protected from flow-induced increases in QO2 under pathophysiological conditions.

scholarly journals Nephron filtration rate and proximal tubular fluid reabsorption in the Akita mouse model of type I diabetes mellitus

F1000Research ◽  
2013 ◽  
Vol 2 ◽  
pp. 83 ◽  
Author(s):  
Jurgen Schnermann ◽  
Mona Oppermann ◽  
Yuning Huang
Keyword(s):  
Diabetes Mellitus ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Type I Diabetes ◽  
Type I ◽  
Fluid Reabsorption ◽  
Single Nephron ◽  
Proximal Tubular ◽  
Tubular Fluid Reabsorption

An increase of glomerular filtration rate (hyperfiltration) is an early functional change associated with type I or type II diabetes mellitus in patients and animal models. The causes underlying glomerular hyperfiltration are not entirely clear. There is evidence from studies in the streptozotocin model of diabetes in rats that an increase of proximal tubular reabsorption results in the withdrawal of a vasoconstrictor input exerted by the tubuloglomerular feedback (TGF) mechanism. In the present study, we have used micropuncture to assess single nephron function in wild type (WT) mice and in two strains of type I diabetic Ins2+/- mice in either a C57Bl/6 (Akita) or an A1AR-/- background (Akita/A1AR-/-) in which TGF is non-functional. Kidney glomerular filtration rate (GFR) of anesthetized mice was increased by 25% in Akita mice and by 52% in Akita/A1AR-/-, but did not differ between genotypes when corrected for kidney weight. Single nephron GFR (SNGFR) measured by end-proximal fluid collections averaged 11.8 ± 1 nl/min (n=17), 13.05 ± 1.1 nl/min (n=23; p=0.27), and 15.4 ± 0.84 nl/min (n=26; p=0.009 compared to WT; p=0.09 compared to Akita) in WT, Akita, and Akita/A1AR-/- mice respectively. Proximal tubular fluid reabsorption was not different between WT and diabetic mice and correlated with SNGFR in all genotypes. We conclude that glomerular hyperfiltration is a primary event in the Akita model of type I diabetes, perhaps driven by an increased filtering surface area, and that it is ameliorated by TGF to the extent that this regulatory system is functional.

scholarly journals Segmental chloride transport in the Dahl-S rat kidney during L-arginine administration.

1995 ◽  
Vol 5 (8) ◽  
pp. 1567-1572
Author(s):  
K A Kirchner ◽  
B A Crosby ◽  
A R Patel ◽  
J P Granger
Keyword(s):  
Sodium Chloride ◽  
Perfusion Pressure ◽  
Chloride Transport ◽  
Rat Kidney ◽  
Renal Perfusion ◽  
Fluid Reabsorption ◽  
Nephron Segments ◽  
Single Nephron ◽  
Chloride Excretion ◽  
Pressure Natriuresis

L-Arginine normalizes pressure natriuresis in Dahl salt-sensitive (DS) rats. The nephron segments responsible for improvement in sodium chloride handling during L-arginine administration are unknown. Micropuncture techniques were used to examine fluid and chloride transport along superficial nephron segments in DS rats maintained on an 8% sodium diet and given L-arginine or vehicle ip for 3 wk. Renal perfusion pressure in vehicle-treated DS rats was reduced to that of L-arginine-treated DS rats with an aortic snare. Dahl salt-resistant (DR) rats receiving vehicle were examined for comparison. In agreement with previous studies, urinary sodium chloride excretion was greater (P < 0.05) in L-arginine DS rats than in vehicle DS rats and not different from DR rats at equivalent renal perfusion pressures. Whole-kidney and single-nephron GFR were not different (P = not significant) among groups. Fractional proximal tubule chloride and fluid reabsorption was not different among groups. Fractional loop chloride reabsorption was greater in vehicle-treated DS rats than in DR rats (58.5 +/- 1.5 versus 46.6 +/- 1.7%; P < 0.05), confirming the enhanced chloride reabsorption at this location in DS rats previously reported. Fractional loop chloride reabsorption was identical in vehicle- and L-arginine-treated DS rats (58.4 +/- 1.4 versus 58.9 +/- 3.9%; P = not significant). Fractional loop fluid reabsorption was not different among groups. Fractional distal fluid and chloride reabsorption was not different between DS rat groups.(ABSTRACT TRUNCATED AT 250 WORDS)

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