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