7 hypertensive patients (H) and 8 normotensive volunteers (N) were loaded with NaCl (4.5 mEq Na +/kg body weight i.v.) during water diuresis (A) and antidiuresis (B). In 6 antidiuretic subjects (3H and 3N) urine volume (V) was progressively raised up to over 30 ml/min, by intravenous infusion (12 ml/min) of hypertonic (3%) saline (C). It is assumed that in (A) CH2O is an index of Na+ reabsorption in short Henle's loops. In (B) and (C) TcH2O is proportional to Na+ reabsorption in long Henle's loops. In (A) CcH2O was significantly lower in H. In (B) TcH2O was similar in H and N. In (C), TcH2O reached an earlier plateau in H than in N. These results demonstrate that exaggerated natriuresis depends on defective Na+ reabsorption in Henle's loops, suggesting that the defect depends upon the transmission of hypertension to medullary circulation. The increase in hemodynamic pressure in vasa recta opposes Na+ reabsorption both in short and in long Henle's loops. However, the effects on TcH2O of the decrease in Na+ reabsorption in long loops is blunted by the greater Na+ delivery, secondary to the increase in GFR, that follows the rise in filtration pressure.