Distal nephron sodium-potassium exchange in children with nephrotic syndrome

2003 ◽  
Vol 59 (04) ◽  
pp. 259-266 ◽  
Author(s):  
R.A.M.G. Donckerwolcke ◽  
A. France ◽  
A. Raes ◽  
J. Vande Walle
1983 ◽  
Vol 244 (1) ◽  
pp. F19-F27
Author(s):  
H. J. Adrogue ◽  
B. J. Stinebaugh ◽  
A. Gougoux ◽  
G. Lemieux ◽  
P. Vinay ◽  
...  

The present studies evaluate the effect of acute hypercapnia on distal nephron H+ secretion (DNH+S) in vivo by means of the urine-blood PCO2 difference (U-B PCO2) in alkaline urine. Bicarbonaturia was induced by either a sodium bicarbonate infusion or L-lysine administration. Our results demonstrate that the U-B PCO2, as a function of the urinary bicarbonate concentration, was significantly lower during acute respiratory acidosis; this effect was not dependent on changes in glomerular filtration rate and/or fractional excretion of sodium, potassium, and chloride. Infusion of the sodium salts of sulfate, a nonreabsorbable anion, did not correct the diminished U-B PCO2. Amiloride caused the U-B PCO2 to fall in normocapnic dogs but not in hypercapnic dogs. When hypercapnia was superimposed in dogs with extracellular fluid volume contraction, there were no changes in the U-B PCO2. This study indicates that acute hypercapnia in the intact dog decreases DNH+S and is compatible with an effect of hypercapnia on the voltage-dependent component of urine acidification. The mechanism appears to be direct rather than secondary to factors that influence the rate of sodium delivery to the distal nephron.


Work on ion transport in plant cells and tissues is largely concerned with the properties of cells rather than of cell layers, and the evidence is on the whole against an important role for asymmetric ion transport across cell layers equivalent to animal epithelia. Cells structurally specialized for transport, having a large increase in surface area, seem to occur singly or in small groups, but not to be organized into closely packed layers; they are known as transfer cells and were described in a wide variety of situations by Gunning & Pate (1969). At the cell level, ion transport is best characterized in giant algal cells, but the situation may well be similar in higher plants. In Nitella translucens an ouabain-sensitive ATP-dependent sodium-potassium exchange pump at the plasmalemma maintains the high K/Na of the cell, and the high internal osmotic pressure is achieved by net salt uptake by a (chloride + cations) pump, also at the plasmalemma. The linkage between chloride and cations seems more likely to be chemical than electrogenic. This pump may be energized by a membrane redox system, but is not ATP-powered. The mechanism for initial entry of chloride to the cell seems also to control the distribution of tracer chloride between cytoplasm and vacuole, since the two processes of entry and transfer to the vacuole are very closely linked. The kinetics of vacuolar transfer are consistent with a pinocytotic entry of salt at the plasmalemma, fusion ofpinocytotic vesicles with the endoplasmic reticulum, from which new vacuole is formed. The process of discharge to the vacuole seems to be quantized, but the mechanism and significance of this observation are not understood.


1980 ◽  
Vol 239 (1) ◽  
pp. H31-H39 ◽  
Author(s):  
M. B. Pine ◽  
D. Kahne ◽  
B. Jaski ◽  
C. S. Apstein ◽  
K. Thorp ◽  
...  

The role of cell membrane permeability to sodium in cell volume regulation during inhibition of the sodium-potassium exchange pump with ouabain and during total metabolic blockade was evaluated in sections of guinea pig renal cortex, ventricle, and atrium incubated in Krebs-Henseleit solution. In all tissues, 2 and 3 h of ouabain and metabolic blockade resulted in similar marked losses of potassium and parallel continuous reductions in resting membrane potentials. Only metabolic blockade of renal cortex increased cell water, chloride, and total monovalent cations (potassium plus sodium) significantly. Compared to ouabain, metabolic blockade markedly increased the rate of cellular washout of 24Na+ from renal cortex (t 1/2 reduced by 47%), which was significantly greater than reductions in t 1/2 from ventricle (16%) and atrium (15%). Thus, inhibition of sodium-potassium exchange pump activity was not sufficient to produce cell swelling unless associated with marked increases in cell membrane permeability to sodium, in which case sodium influx exceeded potassium loss and substantial increases in monovalent cations, chloride, and water occurred.


2011 ◽  
Vol 589 (14) ◽  
pp. 3611-3621 ◽  
Author(s):  
Marc Fila ◽  
Gaëlle Brideau ◽  
Luciana Morla ◽  
Lydie Cheval ◽  
Georges Deschênes ◽  
...  

1978 ◽  
Vol 234 (1) ◽  
pp. F36-F40 ◽  
Author(s):  
A. G. Scicli ◽  
R. Gandolfi ◽  
O. A. Carretero

The site of formation of kinins in the nephron was determined by stop-flow studies in dogs. Klinin, inulin, sodium, potassium concentrations were measured in the fractions collected during the stop-flow procedures. In addition, in three of the 17 stop-flow experiments, kallikrein activity was also measured. The highest kinin concentration after correction for water reabsorption was found in the fractions that were probably trapped in the distal part of the nephron. Either one or two peak was located either in the fraction overlapping (in one instance) or in the fractions coming prior to the fractions with the highest concentration of potassium. This first peak was present in all but one of the stop-flow experiments and was greater than the second peak. The second peak of kinins was found in 13 of the 17 stop-flow exeriments and was located in the fractions with the lowest sodium concentration. Those fractions with the lowest sodium concentration. Those fractions with the lowest sodium concentration also had the highest kallikrein concentration. No evidence of kinin formation was found in the fractions representing the proximal nephron. We conclude, therefore, that kinins are formed in the distal part of the nephron, with the highest concentration found in the last part of the distal nephron and/or in the renal papilla and pelvis.


1977 ◽  
Vol 198 (1133) ◽  
pp. 463-472 ◽  

Results are presented which suggest that the contribution to the membrane potential in frog skeletal muscle evoked by ionic pump activity is made up of two components. One of these is directly related to the ‘electrogenic’ mode of pump action; the other, of similar magnitude, is an indirect effect due to potassium depletion in the lumen of the T -tubular system. The extent of this depletion has been estimated.


1964 ◽  
Vol 206 (4) ◽  
pp. 743-749 ◽  
Author(s):  
Guy Lemieux ◽  
Yves Warren ◽  
Marc Gervais

During simultaneous restriction of sodium and potassium to 1 and 2 mEq/day, respectively, it has been demonstrated that the dog kidney has a remarkable capacity to conserve potassium, the urinary excretion of this ion decreasing rapidly to equal the intake within 4–5 days. Subsequent administration of sodium 100 mEq/day in the form of chloride failed to influence renal conservation of potassium. Equivalent administration of sodium in the form of sulfate or neutral phosphate resulted in a transient but unequivocal increase in urinary excretion of potassium. When desoxycorticosterone 1 mg/kg day was given while high sodium intake and potassium restriction was continued, significant increase in urinary excretion of potassium was observed regardless of the anionic form in which sodium was given. It is suggested that chloride, a readily permeant anion, may prevent significant tubular sodium-potassium exchange. This effect would appear to be overcome when large amount of mineralocorticoid is acting on the renal tubules.


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