Mechanism of proximal NaCl reabsorption in the proximal tubule of the mammalian kidney.
In the mammalian proximal tubule NaCl reabsorption occurs by both passive and active transport processes. Passive NaCl reabsorption occurs in the presence of a high luminal chloride and a low luminal bicarbonate concentration. These anion gradients provide the driving forces for diffusive Na and Cl movement. Na is driven by the lumen positive PD effected by the greater permeability of the tubular wall to Cl than to HCO3. Cl is driven by its high tubular concentration. Passive NaCl reabsorption accounts for only about 10% to 15% of total proximal NaCl transport. The remaining proximal NaCl is reabsorbed by active transport processes and occurs both in the presence or absence of anion gradients reabsorption. Two mechanisms of active NaCl reabsorption participate in active NaCl reabsorption along the proximal tubule. Firstly, active NaCl reabsorption is electrogenic. In the early proximal tubule Na enters to cell coupled to organic solute transport. This Na reabsorption generates a lumen negative PD and effects "coupled" electrogenic NaCl reabsorption. This mechanism is limited by the supply of organic solutes and is blunted by the greater Na than Cl permeability in the proximal tubule; it probably can account for no more than 10% of proximal NaCl reabsorption. In the terminal proximal tubule, the proximal straight tubule, the apical membrane appears to possess a channel for Na entry. This Na reabsorption also generates a lumen negative PD and effects "simple" electrogenic NaCl reabsorption. This mechanism is limited by the low transport capacity of this segment and probably accounts for no more than 5% to 10% of total proximal NaCl reabsorption. The great bulk of proximal NaCl reabsorption occurs along the entire proximal tubule by active, transcellular electroneutral NaCl reabsorption. The precise cellular transport mechanisms responsible for this process are only recently being defined. At the apical membrane parallel ion exchangers are responsible for NaCl entry into the cell. Na enters via the apical membrane Na-H antiporter. Cl most likely crosses the apical membrane by some combination of Cl-OH and Cl-HCO2 exchangers but not via a Cl-HCO3 exchanger. The relative contributions of Cl-OH and Cl-HCO2 exchange have not been defined. There are two important considerations in this question. First is the availbility of OH versus HCO2. Although there is an infinite supply of OH and a small equilibrium supply of HCO2, it is possible that the luminal concentration of HCO2 could be increased by an USL that raises the concentration of HCO2 to a degree sufficient to supply H2CO2 recycling for physiological transcellular Cl transport rates.(ABSTRACT TRUNCATED AT 400 WORDS)
Berry
C A
CA
Department of Physiology, University of California, San Francisco 94143.
Rector
F C
FC
D000818:Animals; D001692:Biological Transport / Q000502:physiology; D001693:Biological Transport, Active / Q000502:physiology; D002463:Cell Membrane Permeability / Q000502:physiology; D006801:Humans; D007687:Kidney Tubules, Proximal / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism; D012965:Sodium Chloride / Q000493:pharmacokinetics*
D012965:Sodium Chloride; D012964:Sodium