Quercetin inhibits left ventricular hypertrophy in spontaneously hypertensive rats and inhibits angiotensin II-induced H9C2 cells hypertrophy by enhancing PPAR-γ expression and suppressing AP-1 activity.
In conclusion, diverse binding affinities of YY1 and its interacting partners to iNOS -1026C/A resulted in differential promoter activity, and potent inhibition of iNOS expression by YY1/AP-1 complex with -1026C may contribute to an enhanced risk for hypertension.
Down-regulation of basal Fos expression at nucleus tractus solitarii underlies restoration of baroreflex response after antihypertensive treatment in spontaneously hypertensive rats.