Major controversy concerning the ascending thin limb of Henle's loop (ATL) centers on the urine concentration mechanism based on the countercurrent multiplier system in the inner medulla of the kidney. This renal tubular segment has specific transport properties which function to dilute the urine without any movement of water across the epithelium. This segment is fundamentally impermeable to water, moderately permeable to urea, and highly permeable to Na+ and Cl-. Whether NaCl is reabsorbed actively in the ATL has long been an important question. While mathematical modelling studies have failed to explain completely how the osmotic gradient in the inner medulla is generated without active NaCl transport in the ATL, the experimental data support the view that active NaCl reabsorption is absent. Recently, we succeeded in measuring the intracellular Na+ concentration by using the fluorescent Na+ indicator sodium-binding benzofuran isophthalate in the in vitro microperfused ATL. Our data suggest that the ATL maintains a low intracellular Na+ concentration by the ouabain-sensitive Na+/K+ ATPase in the basolateral membrane, and that the luminal membrane of the ATL has furosemide-insensitive Na+ permeability. Active Na+ reabsorption estimated in our study amounts to only a few per cents of the net Na+ reabsorption in the ATL. It is therefore suggested that the major role of Na+ extrusion in the ATL cells is to maintain a low cellular Na+ concentration against ambient hyperosmolarity, although small but substantial amount of Na+ is reabsorbed by the furosemide-insensitive Na+ permeability and ouabain-sensitive Na+/K+ ATPase.