Key result
Genetic deletion of ACE2 in C57BL/6 mice induces vascular dysfunction by impairing nitric oxide release and increasing oxidative stress.
Why the study?
Does genetic deletion of ACE2 impair vascular function and redox balance in mice?
Does genetic deletion of ACE2 impair vascular function and redox balance in mice?
Genetic deletion of ACE2 in mice leads to vascular dysfunction driven by reduced nitric oxide bioavailability and increased oxidative stress, highlighting the protective role of ACE2 in vascular homeostasis.
Answers are grounded in this paper and cite their sources.
Should not yet change clinical practice; hypothesis-generating for ACE2 in human vascular disease.
Accumulating evidence indicates that angiotensin-converting enzyme 2 (ACE2) plays a critical role in cardiovascular homeostasis, and its altered expression is associated with major cardiac and vascular disorders. The aim of this study was to evaluate the regulation of vascular function and assess the vascular redox balance in ACE2-deficient (ACE2-/y) animals. Experiments were performed in 20-22 week-old C57BL/6 and ACE2-/y male mice. Evaluation of endothelium-dependent and -independent relaxation revealed an impairment of in vitro and in vivo vascular function in ACE2-/y mice. Drastic reduction in eNOS expression at both protein and mRNA levels, and a decrease in •NO concentrations were observed in aortas of ACE2-/y mice in comparison to controls. Consistently, these mice presented a lower plasma and urine nitrite concentration, confirming reduced •NO availability in ACE2-deficient animals. Lipid peroxidation was significantly increased and superoxide dismutase activity was decreased in aorta homogenates of ACE2-/y mice, indicating impaired antioxidant capacity. Taken together, our data indicate, that ACE2 regulates vascular function by modulating nitric oxide release and oxidative stress. In conclusion, we elucidate mechanisms by which ACE2 is involved in the maintenance of vascular homeostasis. Furthermore, these findings provide insights into the role of the renin-angiotensin system in both vascular and systemic redox balance.
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Rabelo et al. (2016) studied Vascular dysfunction. Genetic deletion of ACE2 vs. Wild-type C57BL/6 mice was evaluated on Vascular function (endothelium-dependent and -independent relaxation). Genetic deletion of ACE2 in C57BL/6 mice induces vascular dysfunction by impairing nitric oxide release and increasing oxidative stress.
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