Adrenomedullin and nitrite levels in children with Bartter syndrome

Balat A., Cekmen M., Yurekli M., Kutlu O., Islek I., Sonmezgoz E., ...Daha Fazla

PEDIATRIC NEPHROLOGY, cilt.15, ss.266-270, 2000 (SCI-Expanded, Scopus)

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 15
  • Basım Tarihi: 2000
  • Doi Numarası: 10.1007/s004670000474
  • Dergi Adı: PEDIATRIC NEPHROLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.266-270
  • Anahtar Kelimeler: adrenomedullin, Bartter syndrome, nitric oxide, VASCULAR REACTIVITY, HYPOTENSIVE PEPTIDE, OXIDE SYNTHASE, L-ARGININE, HYPERTENSION, HEMODYNAMICS, MECHANISM, PATHWAY, CELLS, URINE
  • İnönü Üniversitesi Adresli: Evet

Özet

Children with Bartter syndrome have lower than normal vascular reactivity with normotension in spite of biochemical and hormonal abnormalities which are typical of hypertension. Nitric oxide (NO) is a potent endogenous vasodilator, and plays an important role in the control of vascular tone. Adrenomedullin (AM) is a novel hypotensive peptide originally isolated from human pheochromocytoma. The possible role of NO and PLM in maintaining this reduced vascular reactivity was examined by studying plasma and urinary nitrite, a stable metabolite of NO, and AM levels in ten children with Bartter syndrome, ten healthy controls, and five children with hypokalemia of causes other than Bartter syndrome (pseudo-Bartter). Urinary excretion of nitrite (mu mol/mg urinary creatinine) was 8.9.+/-1.2 in children with Bartter syndrome, 4.7.+/-0.9 in healthy controls, and 2.9.+/-0.8 in pseudo-Bartter (P<0.05). Plasma nitrite levels (mol/l) were 101.9+/-23.4, 59.9+/-14.7, and 65.0+/-29.7, respectively (P>0.05), in the three groups. Urinary excretion of AM (pmol/mg urinary creatinine) was 187+/-40, 65+/-10, and 160+/-50, respectively (P<0.05), in the three groups. Plasma AM levels were 47.4+/-1.8, 39.9+/-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 Bartter patients in the 6th month of therapy. Urinary nitrite and AM levels were still higher in the Bartter patients than in the other groups. We conclude that in Bartter syndrome the increased NO production may be responsible for the reduced vascular response of the disease. Initially, increased levels of AM in Bartter syndrome and pseudo-Bartter may be a compensatory response to acute hypokalemia; however, continuation of a high level of urinary excretion of AM in children with Bartter syndrome may suggest also the possible role of AM in the reduced vascular response of the disease.