Produção Nacional
Revisado por pares
Deposition of collagen perivascular by Angiotensin II action in the aorta independent of hemodynamic effects
2012; Wiley; Volume: 26; Issue: S1 Linguagem: Inglês
10.1096/fasebj.26.1_supplement.525.5
ISSN1530-6860
AutoresKatia Ap. da Silva Viegas, Thais Cristina Souza-Oliveira, Nara Baptistella Rabechi, Aline Goulart de Paiva, Izabel Alves, Raquel Cristina Campos Machado, C Piva, Alvaro Batista Martins, Sílvia Lacchini,
Tópico(s)Peripheral Artery Disease Management
ResumoThe vascular lesions through trophic stimulation of your wall are an important mechanism of action of Angiotensin II (AngII) in extracellular matrix (ECM) by modulation of synthesis x degradation collagen. The aim was to assess whether AngII can act in the ECM by modifying the deposition perivascular collagen (COL) without hemodynamic effects. Mice were treated for 7 and 14 days with subpressor doses of AngII(100ng/kg/min); Losartan(LOS)‐AT1 receptor blocker(20mg/kg/day); Los+Ang; Control (CONT). Measured systolic blood pressure (SBP) and heart rate (HR) by tail plethysmography. Histological sections of aorta were stained with picrosirius to quantify the perivascular COL analyzed in brightfield and polarized light. Results were compared by 2‐way ANOVA p≤0.05. No changes in SBP and HR between groups and nor significant differences of perivascular COL fibers thick (type I‐polarized light) in treated for 7 days but there was a slight increase these in 14 days with AngII(0.56±0.13au) and Los+AngII (0.55±0.14au) compared to CONT(0.49±0.13au) and LOS(0.38±0.04au) significantly reduced the presence of these fibers. In thin COL fibers (type III) there was no difference. The results suggest that the AngII can act on deposition of perivascular COL fibers thick acting in ECM independent of hemodynamic factor through the activation of the AT1 receptor and through other ways for combined treatment. Grant Funding Source : FAPESP ‐ Research Foundation of the State of Sao Paulo
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