Ablation of angiotensin (1-7) receptor Mas in C57Bl/6 mice causes endothelial dysfunction

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Item Type:	Article
Title:	Ablation of angiotensin (1-7) receptor Mas in C57Bl/6 mice causes endothelial dysfunction
Creators Name:	Rabelo, L.A., Xu, P., Todiras, M., Sampaio, W.O., Buttgereit, J., Bader, M., Santos, R.A. and Alenina, N.
Abstract:	The Mas gene codes for an angiotensin (1-7) receptor. There is accumulating evidence that Mas is involved in vascular homeostasis. We have recently backcrossed Mas-knockout mice to two different genetic backgrounds, C57Bl/6 and FVB/N. FVB/NMas-deficient mice exhibited elevation in blood pressure (BP) and impaired endothelial function. In the present study, we aimed to address the question whether this phenotype is strain-specific. Therefore, we evaluated endothelial function in C57Bl/6Mas-deficient mice. Similar to FVB/NMas-knockout animals, Mas-deficiency in C57Bl/6 mice leads to endothelial dysfunction evaluated by the acute BP effect of acetylcholine administration. Measurements of nitric oxide (NO) and reactive oxygen species (ROS) and the systems involved in their metabolism revealed an imbalance between these vasoactive factors in C57Bl/6Mas-knockout mice, which may explain the impairment of endothelial function in these animals. However, endothelial dysfunction was less prominent in Mas-deficient mice on a C57Bl/6 background compared to FVB/N. Moreover, C57Bl/6Mas-deficient mice remained normotensive while FVB/N-based animals exhibited elevated BP. The impairment of endothelium-dependent vasodilatory response to acetylcholine in two different mouse strains with Mas deficiency indicates a key role of Mas in endothelial function by its effects on the generation and metabolism of NO and ROS.
Keywords:	Mas-Deficient Mice, Endothelial Function, Reactive Oxygen Species, Nitric Oxide, Animals, Mice
Source:	Journal of the American Society of Hypertension
ISSN:	1933-1711
Publisher:	Elsevier
Volume:	2
Number:	6
Page Range:	418-424
Date:	November 2008
Official Publication:	https://doi.org/10.1016/j.jash.2008.05.003
PubMed:	View item in PubMed

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