Sympathetic overdrive, activation of
renin angiotensin systems (RAS), and oxidative stress are vitally involved in the pathogenesis of
hypertension and cardiovascular remodeling. We recently identified that vaccarin protected endothelial cell function from oxidative stress or high
glucose. In this study, we aimed to investigate whether vaccarin attenuated
hypertension and cardiovascular remodeling. Two-kidney one-
clip (2K1C) model rats were used, and low dose of vaccarin (10 mg/kg), high dose of vaccarin (30 mg/kg),
captopril (30 mg/kg) were intraperitoneally administrated. Herein, we showed that 2K1C rats exhibited higher systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), left ventricular mass/
body weight ratio, myocardial
hypertrophy or
fibrosis, media thickness, and media thickness to lumen diameter, which were obviously alleviated by vaccarin and
captopril. In addition, both vaccarin and
captopril abrogated the increased plasma
renin,
angiotensin II (Ang II),
norepinephrine (NE), and the basal sympathetic activity. The AT1R
protein expressions,
NADPH oxidase subunit NOX-2
protein levels and
malondialdehyde (MDA) content were significantly increased, whereas
superoxide dismutase (SOD) and
catalase (CAT) activities were decreased in myocardium, aorta, and mesenteric artery of 2K1C rats, both vaccarin and
captopril treatment counteracted these changes in renovascular hypertensive rats. Collectively, we concluded that vaccarin may be a novel complementary therapeutic medicine for the prevention and treatment of
hypertension. The mechanisms for
antihypertensive effects of vaccarin may be associated with inhibition of sympathetic activity, RAS, and oxidative stress.