The distribution of potassium, sodium and chloride across the apical membrane of renal tubular cells: effect of acute metabolic alkalosis

@article{Beck2004TheDO,
  title={The distribution of potassium, sodium and chloride across the apical membrane of renal tubular cells: effect of acute metabolic alkalosis},
  author={Franz-X. Beck and Adolf D{\"o}rge and Roger Rick and Marion Schramm and Klaus Thurau},
  journal={Pfl{\"u}gers Archiv},
  year={2004},
  volume={411},
  pages={259-267}
}
Studies were undertaken to define the effect of acute metabolic alkalosis (hypertonic sodium bicarbonate i.v.) on the chemical gradients for potassium, sodium and chloride across the apical membrane of individual renal tubule cells. Electron microprobe analysis was used on freeze-dried cryosections of the rat renal cortex to measure electrolyte concentrations in proximal tubule cells and in the various cell types of the superficial distal tubule. Analyses were also performed in fluid samples… 
Effect of acute metabolic acidosis on transmembrane electrolyte gradients in individual renal tubule cells
TLDR
In all but intercalated cells acidosis markedly increased cell phosphorus concentration and cell dry weight indicating cell shrinkage and thus diminution of cell potassium content, and the chemical chloride gradient across the contraluminal membrane was markedly depressed by acidosis.
Effect of increased distal sodium delivery on organic osmolytes and cell electrolytes in the renal outer medulla
TLDR
The findings indicate that the primary event underlying stimulation of sodium absorption along the thick ascending limb during increased distal sodium delivery is enhanced entry of sodium across the apical cell membrane.
Quantitative estimation of transmembrane ion transport in rat renal collecting duct principal cells.
TLDR
This approach sets grounds for utilization of experimental measurements of intracellular sodium concentration and cell volume to quantify the ion permeabilities of OMCD principal cells and aids us in understanding the physiology of the adjustment of renal sodium and potassium excretion.
Physiology of the Developing Kidney: Potassium Homeostasis and Its Disorders
TLDR
Because of the many vital processes dependent on potassium homeostasis, multiple complex and efficient mechanisms have developed to regulate the internal distribution of potassium between the intraand extracellular compartments and the external balance between intake and excretion by the kidney and GI tract.
Transcellular sodium transport and basolateral rubidium uptake in the isolated perfused cortical collecting duct
TLDR
The results support the notion that principal, but not intercalated, cells are involved in transepithelial Na+ absorption, and demonstrate that apical Na+ entry and basolateral Na+/K+-AT-Pase activity are closely coupled in principal cells of the rabbit CCD.
Sodium entry routes in principal and intercalated cells of the isolated perfused cortical collecting duct
TLDR
Results indicate that in principal cells amiloride-sensitive sodium channels constitute the predominant pathway for sodium entry across the apical cell membrane, and substantial amounts of sodium enter principal cells across the basolateral cell membranes, probably via Na-H exchange.
Effect of high NaCl intake on Na+ and K+ transport in the rabbit distal convoluted tubule
TLDR
It is concluded that high NaCl intake increases both Na+ reabsorption and K+ secretion by the DCT, associated with an increased Na+−K+-ATPase activity along with increased Na-and-K+ permeabilities of the luminal membrane, and an increase in the K+ permeability of the basolateral membrane.
The renal cortical collecting duct: a secreting epithelium?
TLDR
It is shown that, in the presence of physiological lumen‐to‐bath concentration gradients, and in the absence of endocrine, paracrine and neural regulation, the mouse CCD secretes sodium, which represents a paradigm shift and represents a physiological target for the regulation of sodium handling and for anti‐hypertensive therapeutic agents.
Cell volume regulation in the renal papilla.
TLDR
There is growing evidence that not only transcriptional processes, but also post-transcriptional mechanisms, such as targeting of transport molecules to the plasma membrane, contribute to the successful adaptation of medullary cells to extreme environmental conditions.
Angiotensin II directly stimulates activity and alters the phosphorylation of Na-K-ATPase in rat proximal tubule with a rapid time course.
TLDR
The physiological role for rapid direct activation of Na-K-ATPase is greater control of intracellular sodium during sodium reabsorption.
...
...

References

SHOWING 1-10 OF 55 REFERENCES
Effect of potassium adaptation on the distribution of potassium, sodium and chloride across the apical membrane of renal tubular cells
TLDR
The data suggest that an increment in cell potassium concentration is not a major functional determinant for the increased distal K secretion observed in high-K rats and that the enhanced distal sodium absorption under this condition may be due to a stimulation of the Na exit step across the basolateral cell membrane in excess of the luminal entry step in most distal tubular cell types.
Potassium transport across renal distal tubules during acid-base disturbances.
TLDR
Rats were subjected to metabolic or respiratory acidosis and alkalosis, to combinations of these acid-base disturbances, and to acute K loading, and no evidence was obtained of a consistent reciprocal relationship between rates of distal tubular K and hydrogen secretion.
Effect of acid lumen pH on potassium transport in renal cortical collecting tubules.
TLDR
It is concluded that a decrease in the pH of the tubule fluid of itself inhibits active potassium secretion in this tubule segment, providing an additional explanation for the decrease in potassium excretion found in acidosis.
Effects of graded solute diuresis on renal tubular sodium transport in the rat.
TLDR
It is suggested that the delivery of increased amounts of sodium to the normally unsaturated later parts of the distal tubule and the elevated tubular sodium concentration after saline loading account for the observed stimulation of Distal tubular net sodium transport.
Electron microprobe analysis of intracellular elements in the rat kidney.
TLDR
Differences in the intracellular concentrations of phosphorus, sodium, and chloride between proximal and distal tubular cells are demonstrated, demonstrating the presence of extracellular compartments in these regions.
Effects of changes in electrical potential difference on tubular potassium transport.
To assess directly the role of the transepithelial potential difference (PD) on potassium concentration differences across distal tubular epithelium, continuous and stationary microperfusion
Stimulation of distal potassium secretion by low lumen chloride in the presence of barium.
TLDR
It is postulated that a cotransport mechanism linking potassium and chloride is present in the luminal membrane of distal tubule cells, that this mechanism operates in parallel with a conductive transport pathway for potassium, and that the K-Cl cottransport mechanism is not inhibited by barium.
Element concentrations of renal and hepatic cells under potassium depletion.
TLDR
The decrease in potassium concentrations in distal tubular cells by about 20% does not seem sufficient to explain the marked fall in urinary potassium excretion, and a rise in cellular sodium was insufficient in any cell type to compensate for the loss of potassium.
Effects of flow rate and potassium intake on distal tubular potassium transfer.
TLDR
It is suggested that whenever sodium delivery stimulates distal Tubular potassium secretion it does so by increasing volume distal tubular potasssium secretion and by augmenting the transepithelial electrical potential difference (lumen negative).
Mineralocorticoid regulation of apical cell membrane Na+ and K+ transport of the cortical collecting duct.
TLDR
It is concluded that the acute effect (within 1 day) of mineralocorticoids on Na+ and K+ transport is an increase in the apical membrane Na+ conductance followed by delayed chronic alterations in the Apical cell membrane K+ Conductance and tight junction conductance, thereby resulting in a sustained increased capacity of the tubule to reabsorb Na + and secrete K+.
...
...