Sodium Reabsorption in Nephron

Overview

Sodium reabsorption in the proximal nephron tubule is coupled* with reabsorption of other key solutes and water, and with secretion of hydrogen.

Sodium reabsorption maintains sodium balance, so that sodium intake equals sodium excretion.

– This is one of the most important functions of the kidney because: As the major cation of the extracellular fluid, the amount of sodium determines extracellular fluid volume (because water follows osmotic gradients), and extracellular fluid volume determines plasma volume, blood volume, and blood pressure, which are critical physiological determinants.

Sodium Reabsorption by Segment:

67% of filtered load is reabsorbed in proximal tubule.
25% in thick ascending limb
5% in the early distal tubule
3% in the late distal tubule and collecting duct.
Less than 1% of the filtered load is excreted in the urine.

Early proximal tubule:

Sodium reabsorption is linked to reabsorption of nutrients, inorganic and organic acids, and the secretion of hydrogen.
Transport occurs via two pathways:

– The transcellular pathway, which transports substances through tubule cells; – The paracellular pathway, which moves substances through "leaky" tight junctions between tubule cells.

Sodium-potassium ATPase (aka, pump) actively pumps sodium out of the tubule cell, and brings potassium into it.

– This exchange creates the electrochemical gradient that drives secondary transport of sodium and other solutes across the luminal membrane and into the tubule cell. Luminal membrane cotransporters* couple movement of sodium into the cell with movement of other solutes, including: – Glucose – Amino acids – Inorganic and organic acids. These solutes move out of the cell via facilitated diffusion*.

As a general rule, water follows sodium:

– Transcellularly, it passes through aquaporin 1 channels located on the luminal and basolateral membranes; – Paracellularly, it passes between the tight junctions of tubule cells.

Countertransporter exchanges sodium for hydrogen, which it secretes into the tubular lumen.
Reactions within the cell produce bicarbonate, which is reabsorbed via facilitated diffusion.

Late Proximal Tubule:

Sodium and chloride reabsorption are linked in the late proximal tubule.

– To understand why this is so, consider that most other solutes were reabsorbed within the early proximal tubule; chloride is not, and, therefore, remains in the tubule fluid as it enters the late proximal tubule.

Sodium-potassium pump creates gradient that drives luminal membrane counter transporters:

– One moves sodium into the cell and hydrogen into the lumen. – The other moves chloride into the cell and formate into the lumen (formate ions are metabolic byproducts).

Chloride then passes through the basolateral membrane down its concentration gradient via simple diffusion.
Both sodium and chloride pass through "leaky" tight junctions between the tubule cells; this is another example of the paracellular pathway.

Thick ascending limb:

Sodium reabsorption is linked to potassium and chloride reabsorption.
Sodium-potassium ATPase on basolateral membrane pumps sodium out of cell, potassium into it.
Drives cotransport of sodium, potassium, and chloride into the cell.

In presence of ADH, activity of cotransporter is increased; In presence of Loop diuretics, chloride-binding site is blocked, cotransport ceases, and sodium is not reabsorbed.

Chloride and potassium diffuse out of the cell through the basolateral membrane;

some potassium "leaks" back into the lumen.

Thick ascending limb is impermeable to water.

Early distal tubule:

Sodium and chloride reabsorption are linked.
Sodium-potassium ATPase creates electrochemical gradient that drives cotransport of sodium and chloride from lumen into cell.

– Thiazide diuretics block chloride binding site on contransporter, so sodium is not reabsorbed.

Chloride exits via simple diffusion.
Early distal tubule is impermeable to water.

Late distal tubule and collecting duct:

Principal cells link sodium reabsorption to potassium secretion.
Sodium-potassium ATPase creates electrochemical gradient that drives sodium diffusion via epithelial sodium channels.
Potassium is secreted into lumen.
Aldosterone increases sodium reabsorption and potassium secretion.

Late distal tubule and collecting duct are only permeable to water in presence of ADH*, which increases aquaporin-2 water channels.

Water exits cell via aquaporin 3 and 4 water channels.

– K-sparing diuretics act on late distal tubule and collecting ducts to reduce sodium reabsorption and potassium secretion.

Sodium Reabsorption in Nephron

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