(Hypertension. 2000;36:631.)
© 2000 American Heart Association, Inc.
Colin Johnston - A Celebration |
Proximal Sodium Reabsorption
An Independent Determinant of Blood Pressure Response to Salt
From the Division of Hypertension and Vascular Medicine, CHUV, and Policlinique médicale universitaire, Lausanne, Switzerland.
Correspondence to Dr M. Burnier, MD, Division of Hypertension and Vascular Medicine, Rue P. Decker, CHUV, 1011 Lausanne, Switzerland. E-mail Michel.Burnier{at}chuv.hospvd.ch
Abstract—The purpose of this study was to evaluate the contribution of renal sodium handling by the proximal tubule as an independent determinant of blood pressure responsiveness to salt in hypertension. We measured blood pressure (BP), renal hemodynamics, and segmental renal sodium handling (with lithium used 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 low 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 filtration 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 hemodynamics and proximal sodium reabsorption. When analyzed by tertiles of their BP response to salt, salt-insensitive hypertensive patients of the first tertile disclosed a pattern of adaptation of proximal sodium reabsorption comparable to that of control subjects, whereas the most salt-sensitive patients of the third tertile had an inverse pattern with a high FELi on low salt 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 significantly and independently associated with the salt-induced changes in BP. These results suggest that proximal sodium reabsorption is an independent determinant of the BP response to salt in hypertension.
Key Words: hypertension, renal • human • blood pressure • sodium
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