This Article Full Text (PDF) References Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Calò, L. Articles by Borsatti, A. Search for Related Content PubMed PubMed Citation Articles by Calò, L. Articles by Borsatti, A. Social Bookmarking                         What's this?

Endothelium-Derived Vasoactive Substances in Bartter's Syndrome

Institute of Internal Medicine, Division of Nephrology, University of Padova

Salvatore Cantaro

Institute of Internal Medicine, Division of Nephrology, University of Padova

Alessio Calabrò

Chair of I Medical Pathology, University of Padova, Italy

Francesco Piarulli

Chair of I Medical Pathology, University of Padova, Italy

Monica Rizzolo

Institute of Internal Medicine, Division of Nephrology, University of Padova

Silvana Favaro

Institute of Internal Medicine, Division of Nephrology, University of Padova

Augusto Antonello

Institute of Internal Medicine, Division of Nephrology, University of Padova

Gaetano Crepaldi

Chair of I Medical Pathology, University of Padova, Italy

Arturo Borsatti

Institute of Internal Medicine, Division of Nephrology, University of Padova

An imbalance between endothelium-derived vasoactive substances such as endothelin and endothelium-derived nitric oxide (NO) might be viewed as a possible determinant of vascular hyporeactivity. To check this possibility the authors evaluated the role of endothelin and NO in the reduced vascular reactivity of Bartter's syndrome.

Plasma immunoreactive endothelin (22.07 ±7.06 vs 13.80 ±1.43 pmol/L, P < 0.011), urinary excretion of NO ₂^- (0.28 ±0.10 vs 0.15 ±0.02, µmol/µmol of urinary creatinine, P < 0.01) and NO₃^- (0.17 ±0.07 vs 0.09 ±0.02 µmol/µmol of urinary crea tinine, P < 0.011), and forearm resting blood flow (FRBF) (6.67 ±1.69 vs 4.30 ±0.38 mL/m'/100 mL, P < 0.005) were increased in patients with Bartter's syndrome in comparison with normal controls (C).

No difference in postischemic maximal FBF was found (34.14 ±4.67 vs 31.35 ±2.86 mL/minute/100 mL), while patients showed a slower recovery after peak flow (PF) (77.57 ±61.35 vs 9.42 ±3.69 seconds, P < 0.013). Higher plasma endothelin supports the defect in vascular reactivity of Bartter's syndrome already shown for angiotensin II and norepinephrine and is in keeping with the altered intracellular calcium signaling previously demonstrated by the authors in this syndrome. The increased excretion of NO₂^- and NO₃^- in this syndrome, together with the higher FRBF and the slower recovery of the FBF after PF, argues in favor of an increased NO synthesis in Bartter's syndrome and of assigning it a role in the vascular hyporeactivity of Bartter's syndrome.

Angiology, Vol. 46, No. 10, 905-913 (1995)
DOI: 10.1177/000331979504601005


CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?