Therapeutic Potential of Quercetin to Decrease Blood Pressure: Review of Efficacy and Mechanisms

Department of Nutrition, Exercise, and Health Science, Central Washington University, Ellensburg, WA, USA.
Advances in Nutrition (Impact Factor: 4.71). 01/2012; 3(1):39-46. DOI: 10.3945/an.111.001271
Source: PubMed


Epidemiological studies beginning in the 1990s have reported that intake of quercetin, a polyphenolic flavonoid found in a wide variety of plant-based foods, such as apples, onions, berries, and red wine, is inversely related to cardiovascular disease. More recent work using hypertensive animals and humans (>140 mm Hg systolic and >90 mm Hg diastolic) indicates a decrease in blood pressure after quercetin supplementation. A number of proposed mechanisms may be responsible for the observed blood pressure decrease such as antioxidant effects, inhibition of angiotensin-converting enzyme activity, and improved endothelium-dependent and -independent function. The majority of these mechanisms have been identified using animal models treated with quercetin, and relatively few have been corroborated in human studies. The purpose of this review is to examine the evidence supporting the role of quercetin as a potential therapeutic agent and the mechanisms by which quercetin might exert its blood pressure-lowering effect.

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    • "Moreover, polyphenols have other anti-hypertensive functions beyond their direct antioxidant activity; they promote the induction of detoxifying enzymes, the activation of NO synthase, the reduction in NADPH oxidase activity, and the inhibition of ET-1 expression (Khurana et al., 2013). Among the polyphenols, experimental evidences have shown that quercetin, besides decreasing oxidative stress, may act as an angiotensin-converting enzyme (ACE) inhibitor and may improve the balance between the vasoconstrictor ET-1 and the vasodilator NO (Larson et al., 2012). "
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    ABSTRACT: Recent studies have shown that DNA damage occurs more often in hypertensive patients than non-hypertensive individuals. Here, we analyzed the in vivo effect of pasta containing 30% of tartary buckwheat sprouts (TBSP) on spontaneously hypertensive rats (SHRs) and normotensive Wistar Kyoto rats (WKY) to elucidate if TBSP could have an anti-genotoxic effect in hypertensive animal models. Both SHRs and WKY rats were divided into two groups and fed for six weeks with 5 g of TBSP and durum wheat flour commercial pasta, respectively. Our results showed that a diet rich in TBSP has anti-genotoxic effect. Indeed, SHRs fed with TBSP exhibited a significant decrease in DNA damage (38%) and more efficient DNA repair (84%) compared to SHRs fed with commercial pasta.
    International Journal of Food Sciences and Nutrition 06/2015; 66(5). DOI:10.3109/09637486.2015.1052378 · 1.21 Impact Factor
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    • "It displays a multitude of activities, such as antioxidant, anti-inflammatory and anti-atherogenic activities (Bast and Haenen, 2013; Boots et al., 2008a; Boots et al., 2008b; Edwards et al., 2007; Kleemann et al., 2011). In addition, quercetin has been found to induce vasorelaxation of resistance arteries, which has been shown to potentially reduce blood pressure (Galindo et al., 2012; Khoo et al., 2010; Larson et al., 2012b; Perez-Vizcaino et al., 2002). The exact mechanism by which quercetin causes vasorelaxation is not fully elucidated. "
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    ABSTRACT: The food supplement quercetin is used as self-medication for prostate disorders and is known to induce vasorelaxation. The drug tamsulosin is used in the treatment of benign prostatic hyperplasia. A major side effect of tamsulosin is orthostatic hypotension, mediated by vasorelaxation resulting from α1-adrenoceptor blockade. The overlapping profile prompted us to investigate the pharmacodynamic interaction of quercetin with tamsulosin. Since quercetin is extensively metabolized in the intestines and the liver, the metabolites quercetin-3-glucuronide and 4'O-methyl-quercetin were also examined. Vasorelaxation induced by the compounds was tested in rat mesenteric arteries (average diameter: 360±μm) constricted by the α1-adrenoceptor agonist phenylephrine. Tamsulosin (0.1nM) decreased phenylephrine sensitivity 17-fold (n=10). Quercetin (5, 10 and 20µM) also caused a decrease (2-, 4- and 6-fold respectively) of phenylephrine sensitivity, while 10µM of quercetin-3-glucuronide and 4'O-methyl-quercetin decreased this sensitivity (1.5- and 2-fold) only slightly (n=6). The combination of tamsulosin with quercetin or quercetin metabolites proved to be far more potent than the compounds in isolation. The combination of quercetin, quercetin-3-glucuronide or 4'O-methyl-quercetin with tamsulosin decreased the phenylephrine sensitivity approximately 200-, 35- and 150-fold (n=6). The strong pharmacodynamic interaction between the food supplement quercetin and tamsulosin underlines the potential of the impact of supplement-drug interactions that warrant more research. Copyright © 2014 Elsevier B.V. All rights reserved.
    European Journal of Pharmacology 11/2014; 746C:132-137. DOI:10.1016/j.ejphar.2014.11.006 · 2.53 Impact Factor
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    • "Various active compounds in B. diffusa include punarnavine, ursolic acid, punarnavoside, liriodendrin, eupalitin, eupalitin-3-O-â-D-galactopyranoside, rotenoids like boeravinones A, B, C, D, E, F and G, quercetin, kaempferol, etc. [21], [57]. Among these, quercetin exhibits antioxidant, antihypertrophic and antihypertensive potential in in vitro and in vivo experimental models [58], [59]. Ursolic acid is reported to possess cardioprotective potential via inducing uncoupling of mitochondrial oxidative phosphorylation and reducing mitochondrial H2O2 production [60]. "
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    ABSTRACT: Mitochondrial dysfunction plays a critical role in the development of cardiac hypertrophy and heart failure. So mitochondria are emerging as one of the important druggable targets in the management of cardiac hypertrophy and other associated complications. In the present study, effects of ethanolic extract of Boerhaavia diffusa (BDE), a green leafy vegetable against mitochondrial dysfunction in angiotensin II (Ang II) induced hypertrophy in H9c2 cardiomyoblasts was evaluated. H9c2 cells challenged with Ang II exhibited pathological hypertrophic responses and mitochondrial dysfunction which was evident from increment in cell volume (49.09±1.13%), protein content (55.17±1.19%), LDH leakage (58.74±1.87%), increased intracellular ROS production (26.25±0.91%), mitochondrial superoxide generation (65.06±2.27%), alteration in mitochondrial transmembrane potential (ΔΨm), opening of mitochondrial permeability transition pore (mPTP) and mitochondrial swelling. In addition, activities of mitochondrial respiratory chain complexes (I-IV), aconitase, NADPH oxidase, thioredoxin reductase, oxygen consumption rate and calcium homeostasis were evaluated. Treatment with BDE significantly prevented the generation of intracellular ROS and mitochondrial superoxide radicals and protected the mitochondria by preventing dissipation of ΔΨm, opening of mPTP, mitochondrial swelling and enhanced the activities of respiratory chain complexes and oxygen consumption rate in H9c2 cells. Activities of aconitase and thioredoxin reductase which was lowered (33.77±0.68% & 45.81±0.71% respectively) due to hypertrophy, were increased in BDE treated cells (P≤0.05). Moreover, BDE also reduced the intracellular calcium overload in Ang II treated cells. Overall results revealed the protective effects of B. diffusa against mitochondrial dysfunction in hypertrophy in H9c2 cells and the present findings may shed new light on the therapeutic potential of B. diffusa in addition to its nutraceutical potentials.
    PLoS ONE 04/2014; 9(4):e96220. DOI:10.1371/journal.pone.0096220 · 3.23 Impact Factor
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