Cardiovascular effects of peroxynitrite.

1. Peroxynitrite (PN) is formed in biological systems from the reaction of nitric oxide (*NO) with superoxide (O2(-)*) and both exist as free radicals. By itself, PN is not a free radical, but it can generate nitrogen dioxide (*NO2) and carbonate radical (CO3(-)*) upon reaction with CO2. 2. The reaction of CO2 constitutes a major pathway for the disposition of PN produced in vivo and this is based on the rapid reaction of PN anion with CO2 and the availability of CO2 in both intra- and extracellular fluids. The free radicals *NO2 and CO3(-)*, in combination with *NO, generated from nitric oxide synthase, can bring about oxidation of critical biological targets resulting in tissue injury. However, the reactions of *NO2, CO3(-)* and *NO with carbohydrates, protein and non-protein thiols, phenols, indoles and uric acid could result in the formation of a number of nitration and nitrosation products in the vasculature. These products serve as long-acting *NO donors and, therefore, contribute to vasorelaxant properties, protective effects on the heart, inhibition of leucocyte-endothelial cell interactions and reduction of reperfusion injury. 3. Herein, we review the chemistry of PN, the observations that the effects of PN could be mediated by formation of an *NO donor-like substance and review the physiological and beneficial effects of PN.