Ionic requirements of proximal tubular sodium transport. III. Selective luminal anion substitution

1979 ◽  
Vol 236 (3) ◽  
pp. F268-F277 ◽  
Author(s):  
R. Green ◽  
J. H. Bishop ◽  
G. Giebisch

The effect of substitution of luminal anions on sodium and fluid absorption in rat renal proximal convoluted tubules was studied with continuous luminal microperfusion methods. Substitution of bicarbonate in the control Ringer perfusion fluid by 25 mM acetate reduced net sodium reabsorption by 40%; substitution by chloride reduced it by 25%; and substitution by cyclamate reduced it by 70%. Infusion of acetazolamide reduced net sodium and fluid transport in all cases except chloride-Ringer perfusion. Cyanide added to the perfusion fluid inhibited fluid and sodium movement completely when there was no imposed chloride concentration gradient, but only reduced fluid and solute movement by 68% when a nominal 36 mM transepithelial chloride concentration gradient existed. We conclude from these observations that passive forces for sodium reabsorption can account for a moderate amount of sodium transport, that the effects of acetazolamide in low concentrations are dependent on the presence of bicarbonate in the lumen, and that some anions alter net sodium transport either by reducing the availability of permeant anion for co-transport with sodium or by a direct effect on the sodium and/or chloride transport systems.

1986 ◽  
Vol 250 (4) ◽  
pp. F644-F648
Author(s):  
K. J. Howlin ◽  
R. J. Alpern ◽  
C. A. Berry ◽  
F. C. Rector

One- to two-thirds of NaCl absorption in the late proximal convoluted tubule (no luminal organic solutes present) is inhibited by cyanide and thus is dependent on active transport. To examine whether this active transport-dependent NaCl transport is electrogenic or electroneutral, the effect of cyanide on transepithelial potential difference (PD) was measured in the rat proximal convoluted tubule microperfused in vivo. In the presence of an ultrafiltrate-like luminal perfusate containing glucose and alanine, cyanide addition caused the transepithelial PD to change from -0.44 +/- 0.04 to -0.05 +/- 0.03 mV (P less than 0.001). In the presence of a late proximal tubular fluid (high chloride, low bicarbonate, no organics), the transepithelial PD was 1.23 +/- 0.06 mV and was unchanged at 1.19 +/- 0.05 mV after cyanide addition (NS). To eliminate the possibility that an effect of cyanide on a putative acidification-dependent lumen-positive PD was concealing an effect on an electrogenic sodium transport-dependent lumen-negative PD, the above studies were repeated in the presence of acetazolamide. Cyanide did not affect the transepithelial PD (1.17 +/- 0.05 vs. 1.07 +/- 0.06 mV, NS). We conclude that, although cyanide-inhibitable NaCl transport is electrogenic in the presence of luminal organic solutes, it does not generate a transepithelial PD in their absence and therefore is electroneutral.


1979 ◽  
Vol 57 (4) ◽  
pp. 367-374 ◽  
Author(s):  
Sung-Feng Wen

1. Clearance and micropuncture studies were performed in 19 thyroparathyroidectomized dogs to examine the inter-relationship between the renal transport of sodium, glucose and phosphate. 2. All experiments were carried out before and after the intravenous administration of phlorhizin [7 mg (15 μmol)/kg] with a sustaining infusion of the same dose/h. Thirteen dogs were studied during hydropenia (group I) and six dogs in the volume-expanded state (group II). 3. In the proximal tubule, phlorhizin significantly reduced sodium reabsorption in hydropenic dogs, but had no effect in volume-expanded dogs. Proximal tubular glucose reabsorption was completely inhibited by phlorhizin in both groups, but no significant change in phosphate reabsorption was observed. 4. Fractional glucose excretion in the urine reached 83–89% after phlorhizin, values significantly less than 100%, suggesting a residual reabsorption of glucose in a more distal segment or in deep nephrons. The changes in fractional excretion of sodium and phosphate were significantly correlated. 5. The effect of phlorhizin on both sodium and glucose reabsorption in the proximal tubule in hydropenic dogs suggests the existence of a co-transport mechanism, whereas the absence of an effect on sodium transport in volume-expanded dogs despite complete inhibition of glucose reabsorption indicates the existence of a sodium-independent component of net proximal tubular glucose transport. 6. Absence of the effect of phlorhizin on proximal tubular phosphate transport in the face of a significant reduction in sodium reabsorption implies that the reciprocal relationship between glucose and phosphate transport could be masked by the changes in sodium transport. Thus the sodium-phosphate transport relationship may prevail over that of glucose-phosphate in the proximal tubule.


1970 ◽  
Vol 23 (4) ◽  
pp. 953 ◽  
Author(s):  
JB Robinson ◽  
FA Smith

The influx of 36Cl has been measured in slices of citrus leaves. The influx increases with increasing external chloride concentration. The shape of the influx v. concentration curve depends on the nature and concentration of the accompanying cations (Na+ and K+). There is no evidence for the two distinct chloride transport systems reported by other workers. Chloride influx was not stimulated by light under aerobic conditions and was sensitive to 2,4-dinitrophenol at uncoupling concentrations. Under anaerobic conditions influx was maintained by light but severely limited by dark conditions. 3-(chlorophenyl)-I,I-dimethylurea did not affect aerobic influx and only high levels (5 X 10-OM) affected the anaerobic influx in the light. It is proposed that chloride influx is normally dependent on oxidative phosphorylation but that cyclic photophosphorylation may provide an alternative energy source. The implications of these results are discussed with respect to ionic relations of whole leaves and salinity damage.


1975 ◽  
Vol 229 (5) ◽  
pp. 1205-1215 ◽  
Author(s):  
R Green ◽  
G Giebisch

Simultaneous perfusion of peritubular capillaries and proximal convoluted tubules was used to study the effect of varying transepithelial ionic gradients on ionic fluxes. Results show that net sodium influx and volume flux was one-third of normal when bicarbonate was absent, no chloride gradient existed, and glucose and amino acids were absent. Addition of bicarbonate to the luminal fluid did not restore the flux to normal, but peritubular bicarbonate did restore it. A chloride gradient imposed when no bicarbonate was present could only increase the fluxes slightly, but his flux was significant even after cyanide had poisoned transport. Reversing the chloride concentration gradient decreased the net sodium and volume fluxes whether bicarbonate was present or not. Glucose had no effect on fluxes, but substitution of Na by choline abolished them entirely. It is concluded that sodium is actively transported, that a chloride concentration gradient from lumen to plasma could account for up to 20% of net transport, and that peritubular bicarbonate is necessary for normal rates of sodium and fluid absorption.


2001 ◽  
Vol 81 (1) ◽  
pp. 345-418 ◽  
Author(s):  
Eric Féraille ◽  
Alain Doucet

Tubular reabsorption of filtered sodium is quantitatively the main contribution of kidneys to salt and water homeostasis. The transcellular reabsorption of sodium proceeds by a two-step mechanism: Na+-K+-ATPase-energized basolateral active extrusion of sodium permits passive apical entry through various sodium transport systems. In the past 15 years, most of the renal sodium transport systems (Na+-K+-ATPase, channels, cotransporters, and exchangers) have been characterized at a molecular level. Coupled to the methods developed during the 1965–1985 decades to circumvent kidney heterogeneity and analyze sodium transport at the level of single nephron segments, cloning of the transporters allowed us to move our understanding of hormone regulation of sodium transport from a cellular to a molecular level. The main purpose of this review is to analyze how molecular events at the transporter level account for the physiological changes in tubular handling of sodium promoted by hormones. In recent years, it also became obvious that intracellular signaling pathways interacted with each other, leading to synergisms or antagonisms. A second aim of this review is therefore to analyze the integrated network of signaling pathways underlying hormone action. Given the central role of Na+-K+-ATPase in sodium reabsorption, the first part of this review focuses on its structural and functional properties, with a special mention of the specificity of Na+-K+-ATPase expressed in renal tubule. In a second part, the general mechanisms of hormone signaling are briefly introduced before a more detailed discussion of the nephron segment-specific expression of hormone receptors and signaling pathways. The three following parts integrate the molecular and physiological aspects of the hormonal regulation of sodium transport processes in three nephron segments: the proximal tubule, the thick ascending limb of Henle's loop, and the collecting duct.


1988 ◽  
Vol 119 (2) ◽  
pp. 309-314 ◽  
Author(s):  
J. Pearson ◽  
J. R. Bourke ◽  
S. W. Manley ◽  
G. J. Huxham ◽  
T. Matainaho ◽  
...  

ABSTRACT Confluent monolayers of cultured porcine thyroid cells transport fluid from the apical to the basal surface, forming circumscribed zones of detachment from the culture dish substrate (domes). The transepithelial potential (TEP), positive on the basal side, was 12·9 ± 0·4 (s.e.m.) mV (n = 93) under control conditions, increasing to 38·9 ± 0·3 mV (n = 281) when fluid transport was stimulated by prostaglandin E2 (PGE2; 1 μmol/l). Forskolin (1 μmol/l) and 8-(4-chlorophenylthio) adenosine 3′,5′-cyclic monophosphate (0·5 mmol/l) were also effective in increasing TEP. Addition of amiloride in concentrations sufficient to block fluid transport (100 μmol/l) reduced the TEP to 5·8 ± 0·3 mV (n=76). Substitution of N-methyl-d-glucamine for sodium in the medium reduced the PGE2-stimulated TEP to 13·4 ± 0·8 mV (n = 32). Substitution of gluconate for chloride increased the TEP to 40·3 ± 0·4 mV (n = 160). Removal of bicarbonate or potassium from the medium, or addition of ouabain (200 μmol/l) were also effective in reducing the TEP. In media of low bicarbonate concentration (1 mmol NaHCO3/l), acetazolamide (1 mmol/l) reduced the TEP. Fluid transport by the monolayer as measured by the change in height of domes was increased by PGE2 (1 μmol/l). PGE2-stimulated fluid transport was inhibited by sodium or chloride ion substitution, bicarbonate removal or the addition of ouabain (200 μmol/l) or amiloride (100 μmol/l). It was concluded that fluid transport in thyroid monolayers is mediated by rheogenic sodium transport with chloride transport being passive, electrogenically coupled to sodium transport. Sodium entry to the apical pole of the cells occurs by an amiloride-sensitive mechanism, and sodium extrusion at the basal pole depends on the Na+/K+ ATPase. J. Endocr. (1988) 119, 309–314


1975 ◽  
Vol 229 (5) ◽  
pp. 1216-1226 ◽  
Author(s):  
R Green ◽  
G Giebisch

Simultaneous perfusion to proximal convoluted tubules and peritubular capillaries was used to study the effects of different perfusion fluids on sodium reabsorption and hydrogen secretion, which was calculated as bicarbonate reabsorption and titratable acid. Results show that sodium reabsorption was not tightly coupled to hydrogen secretion. Bicarbonate stimulates both sodium reabsorption and hydrogen secretion, but Tris stimulates only sodium reabsorption. Imposing an adverse chloride gradient across the proximal tubule (C1- peritubular greater than C1- luminal) decreased sodium reabsorption but did not diminish hydrogen secretion. Diamox inhibited both net sodium and hydrogen transport. It is concluded that there is not firm linkage between sodium reabsorption and hydrogen secretion and that bicarbonate probably stimulates sodium transport by a number of mechanisms, including an effect on the sodium transport unrelated to its ability to increase hydrogen ion secretion.


2002 ◽  
Vol 283 (3) ◽  
pp. F525-F531 ◽  
Author(s):  
Raymond Quigley ◽  
Michel Baum

The early proximal tubule preferentially reabsorbs organic solutes and bicarbonate over chloride ions, resulting in a luminal fluid with a higher chloride concentration than that in blood. From this late proximal tubular fluid, one-half of NaCl reabsorption by the adult proximal tubule is active and transcellular and one-half is passive and paracellular. The purpose of the present in vitro microperfusion study was to determine the characteristics of passive chloride transport and permeability properties of the adult and neonatal proximal straight tubules (PST). In tubules perfused with a late proximal tubular fluid, net passive chloride flux was 131.7 ± 37.7 pmol · mm−1 · min−1in adult tubules and −17.1 ± 23.3 pmol · mm−1 · min−1 in neonatal proximal tubules ( P < 0.01). Chloride permeability was 10.94 ± 5.21 × 10−5 cm/s in adult proximal tubules and −1.26 ± 1.84 × 10−5 cm/s in neonatal proximal tubules ( P< 0.05). Thus neonatal PST have a chloride permeability not different from zero and have no net passive chloride transport. Bicarbonate permeability is also less in neonates than adults in this segment (−0.07 ± 0.03 × 10−5 vs. 0.93 ± 0.27 × 10−5 cm/s, P < 0.01). Neonatal PST have higher sodium-to chloride and bicarbonate-to-chloride permeability ratios than adult PST. However, mannitol and sucrose permeabilities were not different in adult proximal tubules and neonatal PST. Transepithelial resistance was measured using current injection and cable analysis. The resistance was 6.7 ± 0.7 Ω · cm2 in adult tubules and 11.3 ± 1.4 Ω · cm2 in neonatal PST ( P < 0.01). In conclusion, there are significant maturational changes in the characteristics of the PST paracellular pathway affecting transport in this nephron segment.


Materials ◽  
2021 ◽  
Vol 14 (14) ◽  
pp. 3975
Author(s):  
Magdalena German ◽  
Jerzy Pamin

Reinforced concrete structures can be strongly damaged by chloride corrosion of reinforcement. Rust accumulated around rebars involves a volumetric expansion, causing cracking of the surrounding concrete. To simulate the corrosion progress, the initiation phase of the corrosion process is first examined, taking into account the phenomena of oxygen and chloride transport as well as the corrosion current flow. This makes it possible to estimate the mass of produced rust, whereby a corrosion level is defined. A combination of three numerical methods is used to solve the coupled problem. The example object of the research is a beam cross-section with four reinforcement bars. The proposed methodology allows one to predict evolving chloride concentration and time to reinforcement depassivation, depending on the reinforcement position and on the location of a point on the bar surface. Moreover, the dependence of the corrosion initiation time on the chloride diffusion coefficient, chloride threshold, and reinforcement cover thickness is examined.


2000 ◽  
Vol 279 (4) ◽  
pp. R1268-R1276 ◽  
Author(s):  
Paul P. Leyssac ◽  
Niels-Henrik Holstein-Rathlou ◽  
Ole Skøtt

Inconsistencies in previous reports regarding changes in early distal NaCl concentration (EDNaCl) and renin secretion during osmotic diuresis motivated our reinvestigation. After intravenous infusion of 10% mannitol, EDNaCl fell from 42.6 to 34.2 mM. Proximal tubular pressure increased by 12.6 mmHg. Urine flow increased 10-fold, and sodium excretion increased by 177%. Plasma renin concentration (PRC) increased by 58%. Renal blood flow and glomerular filtration rate decreased, however end-proximal flow remained unchanged. After a similar volume of hypotonic glucose (152 mM), EDNaClincreased by 3.6 mM, ( P < 0.01) without changes in renal hemodynamics, urine flow, sodium excretion rate, or PRC. Infusion of 300 μmol NaCl in a smaller volume caused EDNaCl to increase by 6.4 mM without significant changes in PRC. Urine flow and sodium excretion increased significantly. There was a significant inverse relationship between superficial nephron EDNaCl and PRC. We conclude that EDNa decreases during osmotic diuresis, suggesting that the increase in PRC was mediated by the macula densa. The results suggest that the natriuresis during osmotic diuresis is a result of impaired sodium reabsorption in distal tubules and collecting ducts.


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