Nitric oxide is a key player in regulating vascular tone. Impaired endothelial nitric oxide synthesis plays an important role in hypertension. Replenishing of nitric oxide by sodium nitrite (NaNO2) has not been investigated in patients with essential hypertension (EHT). We aimed to determine the effects of NaNO2 on blood pressure (BP) and renal sodium and water regulation in patients with EHT compared with healthy control study participants (CON).Methods:
In a placebo-controlled, crossover study, we infused 240 μg NaNO2/kg/h or isotonic saline for 2 h in 14 EHT and 14 CON. During infusion, we measured changes in brachial and central BP, free water clearance, fractional sodium excretion, and urinary excretion rate of γ-subunit of the epithelial sodium channel (U-ENaCγ), and aquaporin-2 (U-AQP2).Results:
Placebo-adjusted brachial SBP decreased 18 mmHg (P < 0.001) during NaNO2 infusion in EHT and 12 mmHg (P < 0.001) in CON (Pbetween = 0.024). Brachial DBP and central SBP decreased equally in both groups during NaNO2. In EHT, we found a decrease in U-ENaCγ during NaNO2 infusion. In both groups, we observed a decrease in fractional sodium excretion, free water clearance, and U-AQP2 during NaNO2 infusion.Conclusion:
This study demonstrated an augmented BP-lowering effect of NaNO2 in patients with EHT. We observed an antinatriuretic and antidiuretic effect of NaNO2 in both groups, and a decrease in U-ENaCγ, solely in EHT. In both groups, we detected a nonvasopressin mediated decrease in U-AQP2, which is most likely compensatory to the decline in diuresis.