DIETARY SODIUM INDUCED INCREASE IN RENAL FUNCTION IS ASSOCIATED WITH AN INCREASE IN NITRITE LEVELS

Abstract

348 Nitric oxide (NO) may play an important role in the regulation of renal function and in the development of sodium-sensitive hypertension. We hypothesized that the increased renal function due to dietary sodium(Na+) loading would be associated with an increase in plasma and urine NO2- levels, in vivo markers of endogenous NO production. To test this hypothesis, seventeen older (63±8 yrs), nondiabetic, moderately obese (34±9% body fat) hypertensives were studied. Subjects were studied at the end of 1-wk of low (20 mEq /d) and high (200 mEq /d) Na+ diets that were identical in composition except for their Na+ content. Renal plasma flow (RPF) and glomerular filtration rate(GFR) were determined by plasma and urinary clearance of 131I-hippuran and 99mTc-DTPA respectively. RPF, GFR, and intra-arterial blood pressure were obtained at the end of each diet. Plasma and urine samples were obtained after a 12-hr fast and NO2- levels were determined using the Griess assay. Plasma NO2- levels increased on the high Na+ diet (25.7±2.5 to 31.8±2.4 μM, P=.06) compared to the low Na+ diet. Although there were no significant changes in GFR or RPF, there was a positive relationship (r=.53, P=.02) between the change in plasma NO2- levels and change in GFR, and the change in plasma NO2- levels and the change in glomerular filtration fraction(GFR/RPF; r=.37, P=.12). The change in RPF was not related to either the change in plasma or urinary NO2- levels. These results suggest that endogenous NO production plays a role in the improvement in GFR induced by dietary Na+ loading. We conclude that impaired NO production may be involved in the inappropriate decline in renal function during dietary Na+ loading. FigureFigure