Intraperitoneal quercetin treatment failed to ameliorate endothelial dysfunction and reduced both NADPH oxidase activity and protein expression of any NADPH oxidase subunits (p47phox, NOX1, and NOX4), suggesting that oral quercetin was superior to intraperitoneal administration for the protection from cardiovascular complications in SHR. The gene discussed is FMO5; the disease is endothelial dysfunction.