Sodium nitrite (NaNO₂) is converted to nitric oxide (NO) in vivo and has vasodilatory and natriuretic effects. Our aim was to examine the effects of NaNO₂ on hemodynamics, sodium excretion and GFR. In a single-blinded, placebo-controlled, cross-over study, we infused placebo (0.9% NaCl) or 0.58, 1.74, or 3.48 μmol NaNO₂/kg/hour for two hours in twelve healthy subjects, after four days standard diet. Subjects were supine and water-loaded. We measured brachial and central blood pressure (BP), plasma concentrations of renin, angiotensin II, aldosterone, arginine vasopressin (P-AVP), and plasma nitrite (P-NO₂^-), GFR by Cr-EDTA clearance, fractional excretion of sodium (FE_Na) free water clearance (C_H2O), and urinary excretion rate of guanosine 3',5'-cyclic monophosphate (U-cGMP). The highest dose reduced brachial systolic BP (5.6 mmHg, p=0.003), central systolic BP (5.6 mmHg, p=0.035) and C_H2O (maximum change from 3.79 to 1.27 ml/min, p=0.031), and increased P-NO₂^- (from 0.065 to 0.766 μmol/l, p<0.001), while reducing U-cGMP (from 444 to 247 pmol/min, p=0.004). GFR, FE_Na, P-AVP and the components in the renin-angiotensin-aldosterone system did not change significantly. In conclusion, intravenous NaNO₂ induced a dose-dependent reduction of brachial and central BP. The hemodynamic effect was not mediated by the renin-angiotensin-aldosterone system. NaNO₂ infusion resulted in a vasopressin-independent decrease in C_H2O and urine output, but no change in urinary sodium excretion or GFR. The lack of increase in cGMP accompanying the increase in NO₂^-, suggests a direct effect of nitrite or nitrate on the renal tubules and vascular bed with little or no systemic conversion to NO.