Abstract：
AIMS:Sickle cell disease (SCD) pathogenesis leads to recurrent vaso-occlusive and hemolytic processes, causing numerous clinical complications including renal damage. As vasoconstrictive mechanisms may be enhanced in SCD, due to endothelial dysfunction and vasoactive protein production, we aimed to determine whether the expression of proteins of the renin-angiotensin system (RAS) may be altered in an animal model of SCD. MAIN METHODS:Plasma angiotensin II (Ang II) was measured in C57BL/6 (WT) mice and mice with SCD by ELISA, while quantitative PCR was used to compare the expressions of the genes encoding the angiotensin-II-receptors 1 and 2 (AT1R and AT2R) and the angiotensin-converting enzymes (ACE1 and ACE2) in the kidneys, hearts, livers and brains of mice. The effects of hydroxyurea (HU; 50-75mg/kg/day, 4weeks) treatment on these parameters were also determined. KEY FINDINGS:Plasma Ang II was significantly diminished in SCD mice, compared with WT mice, in association with decreased AT1R and ACE1 expressions in SCD mice kidneys. Treatment of SCD mice with HU reduced leukocyte and platelet counts and increased plasma Ang II to levels similar to those of WT mice. HU also increased AT1R and ACE2 gene expression in the kidney and heart. SIGNIFICANCE:Results indicate an imbalanced RAS in an SCD mouse model; HU therapy may be able to restore some RAS parameters in these mice. Further investigations regarding Ang II production and the RAS in human SCD may be warranted, as such changes may reflect or contribute to renal damage and alterations in blood pressure.
journal_name
Life Scijournal_title
Life sciencesauthors
dos Santos AF,Almeida CB,Brugnerotto AF,Roversi FM,Pallis FR,Franco-Penteado CF,Lanaro C,Albuquerque DM,Leonardo FC,Costa FF,Conran Ndoi
10.1016/j.lfs.2014.08.021subject
Has Abstractpub_date
2014-11-04 00:00:00pages
7-12issue
1eissn
0024-3205issn
1879-0631pii
S0024-3205(14)00734-6journal_volume
117pub_type
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