The main findings of this study are as follows: (1) both B1- and B2-kinin receptors form heteromers with nNOS and eNOS in thoracic aorta; (2) B1- and B2-kinin receptors equally play an important role in the regulation of endothelium-dependent vasodilation of ACh through nNOS activity; (3) the oxidative stress is closely related with the onset of endothelial dysfunction in aorta of B1R−/− and B2R−/− mice. The gene discussed is NOS1; the disease is endothelial dysfunction.