Sodium transport in the kidney

• sodium in the kidneys is not secreted, it is only reabsorbed
• about 99% of the filtered amount of sodium is reabsorbed

Mechanisms of resorption

• Na + - K + ATPase , located in the basolateral membrane of tubules. Pumps primarily actively (ATP consumption) out into the blood, whereby K + enters the cytoplasm of the tubular cell
• this creates driving forces supporting further sodium transfer:
  • chemical gradient for Na +
    • sodium actively pumped from the tubular cell into the blood causes other sodium to pass from the lumen into the cell according to its gradient
  • electric potential – electric driving force for Na +
    • it is created by actively pumping K + into the tubules, its excess creates a positive charge here, while it is negative in the tubular cell
    • the negative charge pulls more sodium into the cell
• passive flow of Na + into cells – its driving force is the electrochemical gradient. It takes place differently in individual sections of the nephron:
  • proximal tubule
    • resorption of about 65% of the filtered sodium (the concentration of the luminal fluid does not change, because water also leaves with the sodium)
    • about a third of the resorption is active
    • Na + flows passively from the tubule lumen into the tubular cells via:
      • Na + - H + antiport – electroneutral exchange of Na + into the cell and H + into the lumen
      • various cotransport carriers for secondary active transport
        • positively charged particles are removed from the lumen, and therefore a negative charge is created there, the transported cations continue into the blood, where a positive charge is generated - depolarization of the first section of the proximal tubule - the formation of a negative transepithelial potential (LNTP) in the lumen
        • LNTP can be used for paracellular resorption of Cl - into the blood, but this resorption is delayed, so that the luminal concentration of Cl - increases and then diffuses down its gradient, creating a lumen positive transepithelial potential (LPTP)
  • thick segment of the ascending limb of the loop of Henle
    • Na + resorbed by the action of the Na + - 2Cl - - K + transporter
    • transport is primarily electroneutral, but K + are immediately driven back into the lumen, and thus LPTP is formed
  • distal tubule
    • Na + - Cl - cotransport
  • collection channels
    • On channels (activation: ADH , aldosterone , inhibition: ANP , prostaglandins )

On + leaves the cell with

1. Na + - K + ATPase – on the basolateral side
2. Na + - 3HCO 3 - by contransport – tertiary active

Regulation of resorption

• important for maintaining the constancy of the extracellular fluid (individual points connect to each other)

A. lack of salt – hyponatremia (with normal concentration of H 2 O)

• results in a decrease in blood osmolarity
• inhibition of ADH secretion
• increased excretion of water
• reduced volume of extracellular fluid (thus also blood plasma and blood pressure reduction)
• by activating the ARAS (activating reticular ascending system)
• angiotensin induces thirst and, via aldosterone, Na + retention
• secondarily induces water retention (through ADH secreted to increase Na + concentration )

B. an excess of salt

• increased plasma osmolarity
• thirst and stimulation of ADH release
• an increase in the volume of extracellular fluid
• ARAS attenuation
• increased secretion of ANP (atrial natriuretic peptide)
• higher excretion of NaCl and with it H 2 O
• equalization of extracellular fluid volume

Links

References

• GANONG, Wiliam F..  Review of Medical Physiology. 20th edition. Prague 5: Galén, 2005. Vol. 1.  ISBN 80-7262-311-7 .

• TROJAN, Stanislav and Miloš LANGMEIER. Medical Physiology. 4th edition. Prague: Grada Publishing, as, 2003. 722 pp. Vol. 1.  ISBN 80-247-0512-5 .