Epicatechin reduces blood pressure increase in high fructose-fed rats: effects on the determinants of nitric oxide bioavailability

Abstract

This work investigated the blood pressure (BP) lowering effect of the flavanol (─)-epicatechin in a model of metabolic syndrome. Rats were fed a regular chow diet without (Control) or with 10% (w/v) fructose in the drinking water (high fructose, HF) for 8 w. A subgroup of the HF-fed rats was supplemented with (─)-epicatechin 20 mg/kg body weight (HF-EC). Dietary (─)-epicatechin reverted the increase in BP caused by the fructose treatment. In aorta, superoxide anion production and the expression of the NADPH oxidase (NOX) subunits p47phox and p22phox were enhanced in the HF-fed rats. The increase was prevented by (─)-epicatechin. Similar profile was observed for NOX4 expression. The activity of aorta nitric oxide synthase (NOS) was increased in the HF group and was even higher in the HF-EC rats. This effect was paralleled by increased endothelial NOS phosphorylation at the activation site Ser1177. Among the more relevant MAPKs pathways in vascular tissue, JNK was shown to be activated in the aorta of the HF-fed rats and (─)-epicatechin supplementation mitigated this effect. Thus, these results suggest that dietary (−)-epicatechin supplementation prevented hypertension in HF-fed rats decreasing superoxide anion production and elevating NOS activity favoring an increase in NO bioavailability.