IL MECCANISMO DELLA ESAGERATA NATRIURESI NEL SOGGETTO IPERTESO

Seven hypertensive patients (H) and 8 normotensive volunteers (N) were loaded with NaCl (4.5 mEq Na ⁺/kg i.v.) during water diuresis (A) and antidiuresis (B). In 6 antidiuretic subjects (3 H and 3 N) urine volume (V) was progressively raised up to over 30 ml/min, by i.v. infusion (12 ml/min) of hypertonic (3%) saline (C). It is assumed that in (A) C(H2O) is an index of Na ⁺ reabsorption in short Henle's loops. In (B) and (C) T(c)(H2O) is proportional to Na ⁺ reabsorption in long Henle's loops. In (A) C(H2O) was significantly lower in (H). In (B) T(c)(H2O) was similar in H and in N. In (C) T(c)(H2O) 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. During moderate saline load, in fact, C(H2O) (in A), but not T(c)(H2O) (in B), was reduced in H. The increase in hemodynamic pressure in vasa recta would oppose, indeed, Na ⁺ reabsorption both in short and long Henle's loops. The latter, however, belong to nonautoregulating juxtamedullary nephrons. The effects on T(c)(H2O) of the decrease in Na ⁺ reabsorption in long loops is therefore blunted by the greater Na ⁺ delivery, secondary to the increase in GFR, that follows the rise in filtration pressure. The fall in T(c)(H2O) becomes apparent only when the reabsorption capacity of Henle's loops is saturated (in C).