Figure 115

Proximal tubule reabsorptive mechanisms. The proximal tubule is responsible for reabsorption of 60% to 70% of the filtered load of sodium. Reabsorption is accomplished by a combination of both active and passive transport mechanisms that reabsorb sodium and other solutes from the lumen into the lateral spaces and interstitial compartment. The major driving force for this reabsorption is the basolateral sodium-potassium ATPase (Na+-K+ ATPase) that transports Na+ out of the proximal tubule cells in exchange for K+. As in most cells, this maintains a low intracellular Na+ concentration and a high intracellular K+ concentration. The low intracellular Na+ concentration, along with the negative intracellular electrical potential, creates the electrochemical gradient that drives most of the apical transport mechanisms. In the late proximal tubule, a lumen to interstitial chloride concentration gradient drives additional net solute transport. The net solute transport establishes a small osmotic imbalance that drives transtubular water flow through both transcellular and paracellular pathways. In the tubule, water and solutes are reabsorbed isotonically (water and solute in equivalent proportions). The reabsorbed solutes and water are then further reabsorbed from the lateral and interstitial spaces into the peritubular capillaries by the colloid osmotic pressure, which establishes a predominant reabsorptive force as discussed in Figure 1-7. AP—transcapillary hydrostatic pressure gradient; An—transcapillary colloid osmotic pressure gradient.

Regulation of reabsorption

Stimulation Angiotensin II

Adrenergic agents or increased renal nerve activity Increased luminal flow or solute delivery Increased filtration fraction

Inhibition

Volume expansion (via increased backleak) Atrial natriuretic peptide Dopamine

Increased interstitial pressure

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