Fig. 1.

The mechanism of action by which sesamin enhances NO bioactivity in the aortas of spontaneously hypertensive rats (SHR). The sesamin-mediated suppression of eNOS uncoupling, via regulation of DHFR and ONOO- levels, coupled with the stimulatory effect of sesamin on p-eNOS increases NO biosynthesis to relieve endothelial dysfunction and hypertension. Sesamin also inhibits NADPH oxidase, subsequently decreasing superoxide levels and NO oxidative inactivation, contributing to the suppression of endothelial dysfunction and hypertension (adapted from Kong et al., 2015a).