Figure 117

Sodium transport mechanisms in the thick ascending limb of the loop of Henle. The major sodium chloride reabsorptive mechanism in the thick ascending limb at the apical membrane is the sodium-potassium-chloride cotransporter. This electroneutral transporter is inhibited by furosemide and other loop diuretics and is stimulated by a variety of factors. Potassium is recycled across the apical membrane into the lumen, creating a positive voltage in the lumen. An apical sodium-hydrogen exchanger also exists that may function to reabsorb some sodium bicarbonate. The sodium-potassium ATPase (Na+-K+ ATPase) at the basolateral membrane again is the driving force. The basolateral chloride channel and possibly other chloride cotransporters are important in mediating chloride efflux across the basolateral membrane. Sodium and chloride are reabsorbed without water in this segment because water is impermeable across the apical membrane of the thick ascending limb. Thus, the tubular fluid osmolality in this nephron segment is hypotonic.

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