The polyphenol quercetin may prevent CVD due to its antihypertensive and vasorelaxant properties. We investigated the effects of quercetin after regular intake on blood pressure (BP) in overweight-to-obese patients with pre-hypertension and stage I hypertension. In addition, the potential mechanisms responsible for the hypothesised effect of quercetin on BP were explored. Subjects (n 70) were randomised to receive 162 mg/d quercetin from onion skin extract powder or placebo in a double-blinded, placebo-controlled cross-over trial with 6-week treatment periods separated by a 6-week washout period. Before and after the intervention, ambulatory blood pressure (ABP) and office BP were measured; urine and blood samples were collected; and endothelial function was measured by EndoPAT technology. In the total group, quercetin did not significantly affect 24 h ABP parameters and office BP. In the subgroup of hypertensives, quercetin decreased 24 h systolic BP by −3·6 mmHg (P=0·022) when compared with placebo (mean treatment difference, −3·9 mmHg; P=0·049). In addition, quercetin significantly decreased day-time and night-time systolic BP in hypertensives, but without a significant effect in inter-group comparison. In the total group and also in the subgroup of hypertensives, vasoactive biomarkers including endothelin-1, soluble endothelial-derived adhesion molecules, asymmetric dimethylarginine, angiotensin-converting enzyme activity, endothelial function, parameters of oxidation, inflammation, lipid and glucose metabolism were not affected by quercetin. In conclusion, supplementation with 162 mg/d quercetin from onion skin extract lowers ABP in patients with hypertension, suggesting a cardioprotective effect of quercetin. The mechanisms responsible for the BP-lowering effect remain unclear.

K-rich fruit and vegetables may lower blood pressure (BP) and improve vascular function. A randomised controlled trial (ISRCTN50011192) with a cross-over design was conducted in free-living participants with early stages of hypertension (diastolic BP>80 and < 100 mmHg, not receiving BP-lowering medication) to test this hypothesis. Following a 3-week run-in period on a control diet, each subject completed four dietary 6-week dietary interventions (control+placebo capsules, an additional 20 or 40 mmol K+/d from fruit and vegetables or 40 mmol potassium citrate capsules/d) using a Latin square design with a washout period ≥ 5 weeks between the treatment periods. Out of fifty-seven subjects who were randomised, twenty-three male and twenty-five female participants completed the study; compliance to the intervention was corroborated by food intake records and increased urinary K+ excretion; plasma lipids, vitamin C, folate and homocysteine concentrations, urinary Na excretion, and body weight remained were unchanged. On the control diet, mean ambulatory 24 h systolic/diastolic BP were 132·3 (sd 12·0)/81·9 (sd 7·9) mmHg, and changes (Bonferroni's adjusted 95 % CI) compared with the control on the diets providing 20 and 40 mmol K+/d as fruit and vegetables were 0·8 ( − 3·5, 5·3)/0·8 ( − 1·9, 3·5) and 1·7 ( − 3·0, 5·3)/1·5 ( − 1·5, 4·4), respectively, and were 1·8 ( − 2·1, 5·8)/1·4 ( − 1·6, 4·4) mmHg on the 40 mmol potassium citrate supplement, and were not statistically significant. Arterial stiffness, endothelial function, and urinary and plasma isoprostane and C-reactive protein (CRP) concentrations did not differ significantly between the diets. The present study provides no evidence to support dietary advice to increase K intake above usual UK intakes in the subjects with early stages of hypertension.

Fruit and vegetable consumption has been associated with a reduced risk of several diseases including CVD. A part of these effects seen could be linked to anti-inflammatory and antioxidative effects, although this has not been thoroughly investigated. The present study was designed to investigate the effects of the dietary intake of β-carotene, α-tocopherol and ascorbic acid on in vivo biomarkers of inflammation (PGF2α, high-sensitive C-reactive protein (hsCRP) and IL-6 formation) and oxidative stress (F2-isoprostane formation), the two important factors associated with accelerated atherosclerosis. The dietary intake of 704 participants in the Uppsala Longitudinal Study of Adult Men (ULSAM) at age 70 years was registered and inflammatory and oxidative stress biomarkers were quantified 7 years later. The registered dietary intakes of ascorbic acid and α-tocopherol were negatively associated linearly and in quartiles with both PGF2α, hsCRP, IL-6 and F2-isoprostanes, where ascorbic acid intake generally was more strongly associated. Dietary intake of β-carotene was only significantly negatively associated with F2-isoprostanes. In conclusion, the present study is the first to suggest that the intake of food rich in antioxidants is associated with reduced cyclo-oxygenase- and cytokine-mediated inflammation and oxidative stress at 7 years of follow-up. These associations could be linked to the beneficial effects of fruit and vegetables observed on CVD.

Ischaemia reperfusion injury is a common and important phenomenon that occurs predictably in patients undergoing such procedures as cardiopulmonary bypass, thrombolysis, surgery under tourniquet, organ transplantation or embolectomy. Oxidative stress and the resulting lipid peroxidation play a major role in reperfusion injury. Membrane and cellular dysfunction result and, subsequently, organ injury or failure may ensue. Traditional methods of quantifying ischaemia reperfusion injury, including measurement of malondialdehyde, lack specificity and sensitivity. It was reported in 1990 that isoprostanes, a series of prostaglandin-like compounds, are produced by the free radical-catalyzed peroxidation of arachidonic acid. Measurement of the isoprostane concentration in urine or plasma provides the most reliable, non-invasive method currently available to assess oxidative stress in vivo. Serial measurement of isoprostanes in biological fluids has enhanced our understanding of the mechanisms underlying ischaemia reperfusion injury itself and its role in certain diseases. Furthermore, measurement of the isoprostane concentration provides a means to assess the effects of prophylactic and therapeutic interventions. In the future, the development of rapid, simple assays for isoprostanes offers the potential to assess prognosis during and after ischaemia reperfusion events.