is recycled across the apical cell membrane back into the urine. The recirculation of K+ is important to the generation of the electropositive voltage within the lumen, which serves as a driving force for passive transport of Na+, Ca++, and Mg++ through the tight junctions joining adjacent cells. Hence, although K+ is transported by the Na+-K+-2Cl cotransporter, the primary solute absorbed into the blood is NaCl.

Sodium reabsorption in thick ascending limbs depends on the amount, or load, of salt delivered from upstream segments. The amount of sodium reabsorbed by the thick ascending limb increases as more is delivered. In situations such as severe volume contraction, when abnormally large amounts of sodium are reabsorbed by proximal tubules, little sodium reaches the thick ascending limb. In this setting the diuretic action of agents that block Na+-K+-2Cl~ cotransport is impaired. This is attributable to the reduction of sodium in the tubular fluid of the thick ascending limb.

The reabsorption of NaCl by the thick ascending limb is not accompanied by water because of the low hydraulic permeability of this nephron segment. Consequently, the tubular fluid becomes dilute as it passes through the thick ascending limbs. This process contributes to normal urinary dilution. Moreover, when Na+ transport in thick ascending limbs is inhibited, urinary dilution will diminish.

The thick ascending limb is also an important site for the reabsorption of Ca++ and Mg++. These cations are mostly passively reabsorbed through the paracellu-lar pathway between adjacent cells. The driving force for their transport is the transepithelial voltage, which is established by the rate of Na+ reabsorption. Thus, changes in voltage cause proportionate changes in the rate and magnitude of Ca++ and Mg++ reabsorption.

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