Adrenomedullin and nitrite levels in children with Bartter syndrome

Children with Bartter syndrome have lower than normal vascular reactivity w ith normotension in spite of biochemical and hormonal abnormalities which a re typical of hypertension. Nitric oxide (NO) is a potent endogenous vasodi lator, and plays an important role in the control of vascular tone. Adrenom edullin (AM) is a novel hypotensive peptide originally isolated from human pheochromocytoma. The possible role of NO and PLM in maintaining this reduc ed vascular reactivity was examined by studying plasma and urinary nitrite, a stable metabolite of NO, and AM levels in ten children with Bartter synd rome, ten healthy controls, and five children with hypokalemia of causes ot her than Bartter syndrome (pseudo-Bartter). Urinary excretion of nitrite (m u mol/mg urinary creatinine) was 8.9.+/-1.2 in children with Bartter syndro me, 4.7.+/-0.9 in healthy controls, and 2.9.+/-0.8 in pseudo-Bartter (P<0.0 5). Plasma nitrite levels (<mu>mol/l) were 101.9+/-23.4, 59.9+/-14.7, and 6 5.0+/-29.7, respectively (P>0.05), in the three groups. Urinary excretion o f AM (pmol/mg urinary creatinine) was 187+/-40, 65+/-10, and 160+/-50, resp ectively (P<0.05), in the three groups. Plasma AM levels were 47.4+/-1.8, 3 9.9+/-5.9, and 42.4+/-3.9, respectively (P>0.05), in the three groups. The same parameters were repeated in the two groups of controls and in the Bart ter patients in the 6th month of therapy. Urinary nitrite and AM levels wer e still higher in the Bartter patients than in the other groups. We conclud e that in Bartter syndrome the increased NO production may be responsible f or the reduced vascular response of the disease. Initially, increased level s of AM in Bartter syndrome and pseudo-Bartter may be a compensatory respon se to acute hypokalemia; however, continuation of a high level of urinary e xcretion of AM in children with Bartter syndrome may suggest also the possi ble role of AM in the reduced vascular response of the disease.