AI Article Synopsis
- The study investigated the effects of angiotensin 1-7 (ANG 1-7) on blood vessel function in human arterioles, particularly focusing on patients with coronary artery disease (CAD).
- It was found that ANG 1-7 can restore the protective nitric oxide (NO) response in blood vessels from CAD patients, a function that depends on telomerase activity.
- Overall, ANG 1-7 shows potential as a treatment to improve vascular function, highlighting its role in promoting vasodilation and combating the negative effects seen in CAD.
Article Abstract
Objective: This study examined vascular actions of angiotensin 1-7 (ANG 1-7) in human atrial and adipose arterioles.
Approach And Results: The endothelium-derived hyperpolarizing factor of flow-mediated dilation (FMD) switches from antiproliferative nitric oxide (NO) to proatherosclerotic hydrogen peroxide 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 patients with CAD. 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 2-[[(2E)-3-(2-naphthalenyl)-1-oxo-2-butenyl1-yl]amino]benzoic acid. ANG 1-7 dilated arterioles from patients without CAD, whereas dilation was significantly reduced in arterioles from patients with CAD. In atrial arterioles from patients with CAD incubated with ANG 1-7 overnight, the NO synthase inhibitor NG-nitro-l-arginine methyl ester abolished FMD, whereas the hydrogen peroxide scavenger polyethylene glycol catalase had no effect. Conversely, in vessels incubated with ANG 1-7+2-[[(2E)-3-(2-naphthalenyl)-1-oxo-2-butenyl1-yl]amino]benzoic acid, NG-nitro-l-arginine methyl ester had no effect on FMD, but polyethylene glycol 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. Furthermore, ANG 1-7 treatment is sufficient to restore the NO component of FMD in arterioles from patients with CAD in a telomerase-dependent manner.
Conclusions: ANG 1-7 exerts vasoprotection in the human microvasculature via modulation of telomerase activity.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4882242 | PMC |
| http://dx.doi.org/10.1161/ATVBAHA.116.307518 | DOI Listing |
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