Mas receptor deficiency augments angiotensin II-induced atherosclerosis and aortic aneurysm ruptures in hypercholesterolemic male mice

Clinical Relevance: Results from this study suggest a novel mode of intervening in the renin-angiotensin system to treat vascular diseases, namely, by activating Mas receptor (MasR) as the protective arm of the system. Our results demonstrate that when Mas receptors are absent, angiotensin II-induced atherosclerosis and abdominal aortic aneurysms are exacerbated. These results suggest that the endogenous ligand of MasR, angiotensin-(1-7), acts at MasR to counterbalance vascular disease-promoting effects of angiotensin II. Because the development of atherosclerosis and severity of abdominal aortic aneurysms were augmented by MasR deficiency, these results suggest that activation of the MasR pathway may reduce the progressive growth of these dangerous vascular diseases.