A previous report suggested that high salt consumption induces endothelial dysfunction with altered endothelial NO production [20], and trans-ferulic acid significantly potentiated the acetylcholine-induced vascular response of SHR aortas by enhancing the bioavailability of basal and stimulated NO and inhibiting NAD(P)H oxidase [15], a main source of ROS in the vasculature. This evidence concerns the gene FMO5 and endothelial dysfunction.