Background-Angiotensin II (ATII), a potent vasoconstrictor, causes hypertension, promotes infiltration of myelomonocytic cells into the vessel wall, and stimulates both vascular and inflammatory cell NADPH oxidases. Clinical Perspective on p 1381Primary sources of ROS in the cardiovascular system are the Nox-based, multisubunit enzymes NADPH oxidases. 3 Several Nox isoforms are expressed and functional in phagocytic cells like monocytes, macrophages, and neutrophils (myelomonocytic cells); T cells; endothelial cells; vascular smooth muscle cells; and adventitial fibroblasts. All of these have been suggested to contribute to cardiovascular pathology, 3,4 although the importance of individual cell types and their relative impact on the development of cardiovascular disease remain unclear.The phagocytic NADPH oxidase is a major source of ROS elicited by angiotensin II (ATII). 5 In ApoE Ϫ/Ϫ mice fed a high-fat diet, the extent of atherosclerotic lesions is attenuated by limiting the burden of superoxide generated by myelomonocytes. 6 Leukocyte activation by ATII involving the phagocyte-type NADPH oxidase had been demonstrated in

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