NaCl-Induced Renal Vasoconstriction in Salt-Sensitive African Americans

Abstract

Abstract —In 16 African Americans (blacks, 14 men, 2 women) with average admission mean arterial pressure (MAP, mm Hg) 99.9±3.5 (mean±SEM), we investigated whether NaCl-induced renal vasoconstriction attends salt sensitivity and, if so, whether supplemental KHCO 3 ameliorates both conditions. Throughout a 3-week period under controlled metabolic conditions, all subjects ate diets containing 15 mmol NaCl and 30 mmol potassium (K + ) (per 70 kg body wt [BW] per day). Throughout weeks 2 and 3, NaCl was loaded to 250 mmol/d; throughout week 3, dietary K + was supplemented to 170 mmol/d (KHCO 3 ). On the last day of each study week, we measured renal blood flow (RBF) and glomerular filtration rate (GFR) using renal clearances of PAH and inulin. Ten subjects were salt sensitive (SS) (ΔMAP >+5%) and 6 salt resistant (SR). In NaCl-loaded SS but not SR subjects, RBF (mL/min/1.73 m 2 ) decreased from 920±75 to 828±46 ( P <0.05); filtration fraction (FF, %) increased from 19.4± to 21.4 ( P <0.001); and renal vascular resistance (RVR) (10 3 ×mm Hg/[mL/min]) increased from 101±8 to 131±10 ( P <0.001). In all subjects combined, ΔMAP varied inversely with ΔRBF ( r =−0.57, P =0.02) and directly with ΔRVR ( r = 0.65, P =0.006) and ΔFF ( r = 0.59, P =0.03), but not with MAP before NaCl loading. When supplemental KHCO 3 abolished the pressor effect of NaCl in SS subjects, RBF was unaffected but GFR and FF decreased. The results show that in marginally K + -deficient blacks (1) NaCl-induced renal vasoconstrictive dysfunction attends salt sensitivity; (2) the dysfunction varies in extent directly with the NaCl-induced increase in blood pressure (BP); and (3) is complexly affected by supplemented KHCO 3 , GFR and FF decreasing but RBF not changing. In blacks, NaCl-induced renal vasoconstriction may be a pathogenetic event in salt sensitivity.