Frank Holden Mose

Effect of sodium nitrite on renal function, sodium and water excretion and brachial and central blood pressure in healthy subjects. A dose-response study

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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 (FENa) free water clearance (CH2O), 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 CH2O (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, FENa, 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 CH2O 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.

Original languageEnglish
JournalAmerican Journal of Physiology: Renal Physiology
Pages (from-to)F378
Number of pages10
Publication statusPublished - 1 Aug 2017

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