title: Decrease in oxidative stress through supplementation of vitamins C and E is associated with a reduction in blood pressure in patients with essential hypertension.
abstract: Oxidative stress has been associated with mechanisms of EH (essential hypertension). The aim of the present study was to test the hypothesis that the antioxidant properties of vitamins C and E are associated with a decrease in BP (blood pressure) in patients with EH. A randomized double-blind placebo-controlled clinical trial was conducted in 110 men with grade 1 EH (35-60 years of age without obesity, dyslipidaemia and diabetes mellitus, non-smokers, not undergoing vigorous physical exercise, without the use of any medication and/or high consumption of fruit and vegetables). Participants were randomly assigned to receive either vitamins C+E [vitamin C (1 g/day) plus vitamin E (400 international units/day)] or placebo for 8 weeks. Measurements included 24 h ambulatory BP and blood analysis of oxidative-stress-related parameters in erythrocytes (GSH/GSSH ratio, antioxidant enzymes and malondialdehyde) and plasma [FRAP (ferric reducing ability of plasma)], and levels of 8-isoprostane, vitamins C and E were measured at baseline and after treatment. Following administration of vitamins C+E, patients with EH had significantly lower systolic BP, diastolic BP and mean arterial BP and higher erythrocyte and serum antioxidant capacity compared with either placebo-treated patients with EH or the patients with EH at baseline prior to treatment. BP correlated positively with plasma 8-isoprostane levels and negatively with plasma FRAP levels in the vitamins C+E- and placebo-treated groups. In conclusion, the present study supports the view that oxidative stress is involved in the pathogenesis of EH, and that enhancement of antioxidant status by supplementation with vitamins C and E in patients with EH is associated with lower BP. This suggests intervention with antioxidants as an adjunct therapy for hypertension.
authors.affiliation: Laboratory of Renal Pathophysiology, Molecular and Clinical Pharmacology Program, Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, Santiago, Chile. rrodrigo@med.uchile.cl
authors.forename: Ramón
authors.initials: R
authors.lastname: Rodrigo
authors.forename: Hernán
authors.initials: H
authors.lastname: Prat
authors.forename: Walter
authors.initials: W
authors.lastname: Passalacqua
authors.forename: Julia
authors.initials: J
authors.lastname: Araya
authors.forename: Jean P
authors.initials: JP
authors.lastname: Bächler
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D000975:Antioxidants / Q000032:analysis / Q000627:therapeutic use*; D001205:Ascorbic Acid / Q000097:blood / Q000627:therapeutic use*; D001795:Blood Pressure Determination; D015237:Dinoprost / Q000031:analogs & derivatives / Q000097:blood; D004311:Double-Blind Method; D004912:Erythrocytes / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000188:drug therapy*; D007501:Iron / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D016896:Treatment Outcome; D014810:Vitamin E / Q000097:blood / Q000627:therapeutic use*; D014815:Vitamins / Q000097:blood / Q000627:therapeutic use*
chemical_list: D000975:Antioxidants; D014815:Vitamins; D014810:Vitamin E; C075750:8-epi-prostaglandin F2alpha; D015237:Dinoprost; D007501:Iron; D001205:Ascorbic Acid