NaCl-induced renal vasoconstriction in salt-sensitive African Americans - Antipressor and hemodynamic effects of potassium bicarbonate

In 16 African Americans (blacks, 14 men, 2 women) with average admission me an arterial pressure (MAP, mm Hg) 99.9 +/- 3.5 (mean+/-SEM), we investigate d whether NaCl-induced renal vasoconstriction attends salt. sensitivity and , if so, whether supplemental KHCO3 ameliorates both conditions. Throughout a 3-week period under controlled metabolic conditions, all subjects ate di ets 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; thro ughout week 3, dietary K+ was supplemented to 170 mmol/d (KHCO3). On the la st day of each study week, we measured renal blood flow (RBF) and glomerula r filtration rate (GFR) using renal clearances of PAH and inulin. Ten subje cts were salt sensitive (SS) (Delta MAP > +5%) and 6 salt resistant (SR). I n 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) X mm Hg/[mL/min]) increased from 101 +/- 8 to 131 +/- 10 (P < 0.001). I n all subjects combined, Delta MAP varied inversely with Delta RBF (r=-0.57 , P=0.02) and directly with Delta RVR (r- = 0.65, P = 0.006) and Delta FF ( r = 0.59, P = 0.03), but not with MAP before NaCl loading. When supplementa l KHCO3 abolished the presser effect-of NaCl in SS subjects, RBF was unaffe cted but GFR and FF decreased. The results show that in marginally K+-defic ient blacks (1) NaCl-induced renal vasoconstrictive dysfunction attends sal t sensitivity; (2) the dysfunction varies in extent directly with the NaCl- induced increase in blood pressure (BP); and (3) is complexly affected by s upplemented KHCO3, GFR and FF decreasing but RBF not changing. In blacks, N aCl-induced renal vasoconstriction may be a pathogenetic event in salt sens itivity.