In our previous studies on atherosclerotic animal models and in patients with hypertension and dyslipidemia, we showed that treatment with irbesartan, an AT1 receptor antagonist, diminished total MV levels in peripheral blood, especially specific MVs (leukocyte-, platelet-, and endothelial-derived MVs), and increased EPC levels, thereby preventing the development of vascular endothelial dysfunction by the augmentation of endothelium-mediated vasodilation [38,42,43,44]. This evidence concerns the gene AGTR1 and metabolic syndrome.