Quercetin is a polyphenolic flavonoid. Common sources in the diet are apples, onions, berries, and red wine. Epidemiological studies have found an inverse relationship between dietary quercetin intake and cardiovascular disease. This has led to in vitro, in vivo, and clinical research to determine the mechanism by which quercetin exerts cardioprotective effects. Recent studies have found a reduction in blood pressure when hypertensive (>140 mm Hg systolic and >90 mm Hg diastolic) animals and humans are supplemented with quercetin. Proposed mechanisms for the antihypertensive effect of quercetin include decreased oxidative stress, inhibition of angiotensin converting enzyme activity, improved endothelial function, direct action on the vascular smooth muscle, and/or modulation in cell signaling and gene expression. Although in vitro and in vivo evidence exists to support and refute each possibility, it is likely that quercetin influences multiple targets via a combination of known and as yet undiscovered mechanisms. The purpose of this review is to examine the mechanisms whereby quercetin might reduce blood pressure in hypertensive individuals.
Keywords: angiotensin converting enzyme; antioxidants; endothelial function; hypertension; quercetin.