To better understand the role water and urea fluxes play in the urine concentrating mechanism, we determined transepithelial osmotic water (P_f) and urea (P_urea) permeabilities in isolated perfused Munich-Wistar rat long-loop descending (DTL) and ascending (ATL) thin limbs. Thin limbs were isolated either from 0.5 to 2.5 mm below the outer medulla (OM) (upper inner medulla; IM_upper) or from the terminal 2.5 mm of the IM (IM_lower). Segment types were characterized on the basis of structural features and gene expression levels of the water channel aquaporin 1 (AQP1), which was high in DTL_upper, absent in DTL_lower, and absent in ATLs and the chloride channel ClCK1, which was absent in DTLs and high in ATLs. DTL_upper P_f (μm/s) was high (32045 ± 450.28) whereas DTL_lower showed very little or no osmotic water permeability (207.8 ± 241.3). Munich-Wistar rat ATLs have previously been shown to exhibit no water permeability. DTL_upper P_urea (x 10^-5 cm/s) was 40.0 ± 7.3 and much higher in DTL_lower (203.8 ± 30.3), ATL_upper (203.8 ± 35.7) and ATL_lower (265.1 ± 49.8). Phloretin (0.25 mM) did not reduce DTL_upper P_urea, suggesting that P_urea is not due to the urea transporter UT-A2, which is expressed in short-loop DTLs and short portions of some inner medullary DTLs close to the OM. In summary, P_urea is similar in all segments having no osmotic water permeability but is significantly lower in DTL_upper, a segment having high osmotic water permeability. These data are inconsistent with the passive mechanism as originally proposed.