Proximal sodium reabsorption - An independent determinant of blood pressure response to salt

The purpose of this study was to evaluate the contribution of renal sodium handling by the proximal tubule as an independent determinant of blood pres sure responsiveness to salt in hypertension. We measured blood pressure (BP ), renal hemodynamics, and segmental renal sodium handling (with lithium us ed as a marker of proximal sodium reabsorption) in 38 hypertensive patients and 27 normotensive subjects (15 young and 12 age-matched) on a high and l ow sodium diet. In control subjects, changing the diet from a low to a high sodium content resulted in no change in BP and increases in glomerular fil tration rate (P<0.05), renal plasma flow (P<0.05), and fractional excretion of lithium (FELi, P<0.01). In hypertensive patients, comparable variations of sodium intake induced an increase in BP with no change in renal hernody namics and proximal sodium reabsorption. When analyzed by tertiles of their BP response to salt, salt-insensitive hypertensive patients of the first t ertile disclosed a pattern of adaptation of proximal sodium reabsorption co mparable to that of control subjects, whereas the most salt-sensitive patie nts of the third tertile had an inverse pattern with a high FELi on low sal t and a lower FELi on high salt, suggesting an inappropriate modulation of proximal sodium reabsorption. The BP response to salt correlated positively with age (r=0.34, P=0.036) and negatively with the changes in FELi, (r= -0 .37, P=0.029). In a multivariate analysis, the changes in FELi were signifi cantly and independently associated with the salt-induced changes in BP. Th ese results suggest that proximal sodium reabsorption is an independent det erminant of the BP response to salt in hypertension.