Ferder León, Inserra Felipe, Martínez-Maldonado Manuel
Department of Physiology, Ponce School of Medicine, Dr. Ana Perez Marchand Street, PO Box 7004, Ponce, PR00732-7004, USA.
Curr Hypertens Rep. 2006 Jun;8(3):191-8. doi: 10.1007/s11906-006-0050-7.
Excess body weight, high blood pressure, and insulin resistance together have been denominated the metabolic syndrome. In this review, we analyze the potential role of angiotensin II (Ang II) and reactive oxygen species in mediating inflammation in the metabolic syndrome. Ang II induces pro-inflammatory genes and other pro-inflammatory substances and increases oxidative stress that could damage endothelium, myocardium, and renal tissue. Activation of nuclear factor-kappaB and NAD(P)H oxidase are fundamental steps in these pro-inflammatory mechanisms in which intramitochondrial oxidative stress could play a critical role. This sequence of events might explain why reduction in Ang II synthesis by angiotensin-converting enzyme inhibitors (ACEIs) and Ang II type 1 (AT1) receptor blockers (ARBs) have a protective effect against cardiovascular disease.