Review: Interaction among angiotensin II, nitric oxide and oxidative stress

JRAAS 2001;2 (suppl 1):S59-S63 Introduction Many vasoactive substances, such as nitric oxide (NO), endothelin 1 (ET-1), angiotensin II (Ang II), and superoxide anion (O2-) participate in the regulation of cardiovascular function. The balance between these molecules may play a crucial role in maintenance of cardiovascular homeostasis. In most circumstances, NO is an important molecule in terms of cardiac and vascular protection. NO produced by the endothelium modulates vasomotor tone and inhibits platelet aggregation and smooth muscle cell and mesangial cell proliferation. It has also been suggested to have antiatherogenic properties. Ang II, on the other hand, is a powerful vasoconstrictor peptide that has antinatriuretic and prothrombogenic properties. Increased Ang II or overexpression of the Ang II type 1(AT1)-receptor is associated with vascular remodelling in some pathological conditions. O2and other reactive oxygen species (ROS) are often regarded as deleterious molecules. O2can increase vascular constriction, promote growth, and induce oxidant injury. Under normal physiological conditions, O2can be effectively scavenged by antioxidants such as O2dismutase (SOD), which will minimise oxidative damage.Excessive O2interacts with NO to reduce NO bioavailability and generate peroxynitrite, which can induce cardiovascular oxidative injury.