Increased urinary NO2−/NO3− and cyclic guanosine monophosphate levels in patients with bartter's syndrome: Relationship to vascular reactivity

Abstract Nitric oxide (NO) is a potent endogenous vasodilator and plays a pivotal role in the control of vascular tone by the formation of cyclic guanosine monophosphate (GMP). Patients affected by Bartter's syndrome have lower than normal vascular reactivity with normohypotension and decreased peripheral resistances in spite of biochemical and hormonal abnormalities typical of hypertension, and it is possible that increased production of NO may be involved in maintaining this reduced vascular response and vasodilatation. We have examined this possibility by studying NO 2 − /NO 3 − and cyclic GMP urinary excretions to assess NO production in vivo in seven patients affected by Bartter's syndrome compared with seven healthy controls. A group of five patients with hypokalemia other than Bartter syndrome (pseudo-Bartters) was also included in the study to evaluate the effect of hypokalemia on NO production. NO 2 − /NO 3 − urinary excretion (0.45 ± 0.14 v 0.25 ± 0.04 μmol/μmol urinary creatinine [controls], P v 0.28 ± 0.05 [pseudo-Bartters], P v 0.022 ± 0.01 μmol/μmol of urinary creatinine [controls], P v 0.024 ± 0.004 [pseudo-Bartters], P P 2 − /NO 3 − and cyclic GMP urinary excretions point to an increased NO synthesis, which could account for the reduced vascular response of the disease, therefore adding its role in determining the vascular hyporeactivity of Bartter's syndrome.