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10.1161/ATVBAHA.116.307518

http://scihub22266oqcxt.onion/10.1161/ATVBAHA.116.307518
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C4882242!4882242!27079876
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suck abstract from ncbi


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pmid27079876      Arterioscler+Thromb+Vasc+Biol 2016 ; 36 (6): 1254-62
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  • Vascular Actions of Angiotensin 1?7 in the Human Microcirculation ? Novel Role for Telomerase #MMPMID27079876
  • Durand MJ; Zinkevich NS; Riedel M; Gutterman DD; Nasci VL; Salato VK; Hijjawi JB; Reuben CF; North PE; Beyer AM
  • Arterioscler Thromb Vasc Biol 2016[Jun]; 36 (6): 1254-62 PMID27079876show ga
  • Objective: This study examined vascular actions of angiotensin 1?7 (ANG 1?7) in human atrial and adipose arterioles. Approach and Results: The endothelial-derived hyperpolarizing factor of flow mediated dilation (FMD) switches from anti-proliferative nitric oxide (NO) to pro-atherosclerotic hydrogen peroxide (H2O2) in arterioles from humans with coronary artery disease (CAD). Given the known vasoprotective properties of ANG 1?7, we tested the hypothesis that overnight ANG 1?7 treatment restores the NO-component of FMD in arterioles from CAD patients. Endothelial telomerase activity is essential for preserving the NO-component of vasodilation in the human microcirculation, thus we also tested whether telomerase activity was necessary for ANG 1?7 mediated vasoprotection by treating separate arterioles with ANG 1?7 ± the telomerase inhibitor BIBR-1532. ANG 1?7 dilated arterioles from patients without CAD, whereas dilation was significantly reduced in arterioles from CAD patients. In atrial arterioles from CAD patients incubated with ANG 1?7 overnight, the NO synthase inhibitor L-NAME abolished FMD while the H2O2 scavenger PEG catalase had no effect. Conversely, in vessels incubated with ANG 1?7 + BIBR-1532, L-NAME had no effect on FMD but PEG catalase abolished dilation. In cultured human coronary artery endothelial cells, ANG 1?7 significantly increased telomerase activity. These results indicate that ANG 1?7 dilates human microvessels, and dilation is abrogated in the presence of CAD. Further, ANG 1?7 treatment is sufficient to restore the NO component of FMD in arterioles from CAD patients in a telomerase-dependent fashion. Conclusion: ANG 1?7 exerts vasoprotection in the human microvasculature via modulation of telomerase activity.
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