Two models of ypertonic urine formation in the inner medulla were tested. The active model asserts that thin ascending limbs of Henle's loop (ALH) reasorb NaCl hypertonically by active transport; the passive model suggests the reabsorption is by diffusion down a concentration gradient. Using (Na+) in ascending vasa recta (AVR) as a measure of interstitial (Na+), we found no concentration difference between loop tubular fluid and AVR, when the comparison was made at the bend of the loop, or at an ALH sampling site 1 mm from the bend; the results were the same in antidiuresis and saline diuresis. In saline diuresis with flow of tubular fluid to the ALH slowed by simultaneous collection at the bend of the loop,ALH (Na+) fell below AVR levels, a result consistent with active transport, but not with a purely passive mechanism. Although contragradient transport was shown only with flow slowed and the corticomedullary gradient reduced, a model suggests the active component contributes almost half the observed Na+ flux in antidiuresis.

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