Therapeutic Potential of Quercetin to Decrease
Blood Pressure: Review of Efficacy
Abigail J. Larson,3J. David Symons,4and Thunder Jalili4*
3Department of Nutrition, Exercise, and Health Science, Central Washington University, Ellensburg, WA;4Division of Nutrition, University of Utah,
Salt Lake City, UT
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. Adv. Nutr. 3: 39–46, 2012.
The American Heart Association estimates that 74.5 million
Americans have hypertension (1), which is most commonly
defined as systolic blood pressure >140 mm Hg and diastolic
blood pressure >90 mm Hg. Equally alarming are recent
estimates that w25% of the US population has prehyperten-
sion, which is defined as untreated blood pressure of
120–139 mm Hg systolic or 80–89 mm Hg diastolic (1). Al-
though hypertension can frequently exist with other cardio-
vascular disease (CVD)5risk factors such as metabolic
syndrome, it is usually asymptomatic. Importantly, there is
a positive and direct correlation between hypertension and
the risk of other CVDs such as cardiac arrhythmia, coronary
artery disease, cardiac hypertrophy, myocardial infarction,
and heart failure (1). Taken together, it is estimated that,
in 2010, the total direct and indirect costs of CVD was
$503.2 billion (1).
Blood pressure is controlled by neural mechanisms car-
ried out by the autonomic nervous system and humoral
mechanisms involving substances such as nitric oxide
(NO) and endothelin-1 (ET-1) that are released by different
cell types. Decreased vasodilation, increased vasoconstric-
tion, and greater vascular peripheral resistance characterize
hypertension. Treatment of hypertension depends on the
etiology of the disease and includes diet alterations, weight
loss, exercise, and pharmacological interventions. Pharma-
cological therapies [e.g., angiotensin-converting enzyme
(ACE) inhibition, diuretics, and calcium channel blockers]
to treat hypertension are successful but may be associated
with negative side effects such as persistent cough, dry
throat, allergic reactions, dizziness, angioedema, and kidney
failure (2). Lifestyle interventions (either alone or in combi-
nation) such as reduced sodium intake (3), the Dietary In-
terventions to Stop Hypertension diet (4), and increased
physical activity (5) are also known to decrease blood pres-
sure in hypertensive patients. Dietary antioxidant vitamins
and supplements have also been reported to decrease blood
pressure in both animals and humans. For example, both
human and animal studies have used vitamins C (6,7) and
E (8,9) and polyphenolic flavonoids (10–13) to decrease
blood pressure and improve endothelial function. With re-
gard to polyphenolic flavonoids, several epidemiological
1A.J.L. was supported by a grant from University of Utah PEAK Academy J.D.S. was
supported by American Diabetes Association Research Grant 7-08-RA-164, and National
Institutes of Health grant R15 HL 091493-01. T.J. was supported by a University of Utah
College of Health grant, Melaluca Inc. Clinical Research Contract.
2Author disclosures: A.J. Larson, J.D. Symons, and T. Jalili, no conflicts of interest.
5Abbreviations used: ACE, angiotensin-converting enzyme; CVD, cardiovascular disease; ET-1,
endothelin-1; NO, nitric oxide; RAAS, renin-angiotensin-aldosterone system.
*To whom correspondence should be addressed. E-mail: Thunder.Jalili@utah.edu.
ã2012 American Society for Nutrition. Adv. Nutr. 3: 39–46, 2012; doi:10.3945/an.111.001271.
studies found significant correlations between flavonoid in-
take and CVD. Evidence from the Zutphen Elderly Study
suggests a strong cardioprotective effect of several flavo-
noids, including quercetin (14). In this study, the risk of
death from coronary heart disease was decreased by as
much as 68% in men who consumed >29 mg of flavonols
daily compared with men who consumed <10 mg of flavo-
nols daily (14). Although the specific association between
quercetin intake and blood pressure was not examined in
this study, the authors did report an inverse relationship be-
tween foods high in quercetin and blood pressure. Similarly,
other studies examining flavonoids found that increased fla-
vonoid intake is inversely related to chronic disease, such as
CVD (15–18). Given the public interest in alternative ther-
apies for chronic disease coupled with the increasing num-
ber of studies reporting beneficial effects of natural
products on prevention of disease, it is not surprising that
vitamins and polyphenolic flavonoids have become increas-
ingly popular in the treatment and prevention of hyperten-
sion among the public.
One particular flavonoid, quercetin, has been studied in
cell-based assays, experimental animal models, and human
clinical trials in recent years and is gaining popularity as a
natural therapy for hypertension and vascular health. The
purpose of this review is to examine the existing evidence
that may support the use of quercetin as an antihypertensive
agent and to review the possible mechanisms by which quer-
cetin might decrease blood pressure.
Current status of knowledge
Quercetin: Food sources, chemistry, and health benefits
Phytochemicals are produced in plants and have innate bio-
logical activity to protect the plant against insect invasion,
ultraviolet light damage, infection, and diseases. Plants
also derive characteristics of color, flavor, and aroma from
phytochemicals. Flavonoids constitute a class of phytochem-
ical and are divided into various subclasses based on their
molecular structure. The contributions of flavonoids to
health are in part based on their molecular structure (19).
Quercetin is a flavonol and is widely found in many plant-
based foods such as apples, onions, citrus fruits, berries,
red grapes, red wine, broccoli, bark roots, flowers, and tea
(20) (Table 1). The average Western diet supplies 15–40
mg/d of quercetin, and dietary levels >33 mg/d have been as-
sociated with a decreased risk of CVD (14,16,17). Although
the quercetin content of the diet may be estimated using da-
tabases available from the USDA (20), there is some variabil-
ity in the reported flavonoid content of foods because of
variations in soil, harvest, and storage conditions (21). At
present, quercetin supplements are widely available through
commercial sources in doses ranging from 250 to 1500 mg
of quercetin. Typically, these commercial sources use 1 or
more of the various isoforms of quercetin such as quercetin
aglycone, rutin, and other glycoside versions. In general,
quercetin supplements are marketed to the public as alterna-
tive therapy for treating allergies, asthma, bacterial infec-
tions, arthritis, gout, eye disorders, hypertension, and
neurodegenerative disorders. Because few controlled, ran-
domized trials have been performed, there is a lack of data
to provide a solid scientific basis for many of these treatment
claims. However, with regard to hypertension, there is a
body of evidence from cell-based assays, experimental ani-
mal models, and human clinical trials that supports a possi-
ble therapeutic role for quercetin in the treatment of
Bioavailability and safety of quercetin
The chemical structure of pure quercetin is an unconjugated
aglycone that does not have a carbohydrate moiety (Fig. 1).
Quercetin in foods, such as onions, has a sugar group in its
structure, which is known as a glycoside form (Fig. 2). Sup-
plemental forms of quercetin are usually quercetin aglycone,
although some products have small amounts of a glycoside
called rutin as well. The bioavailability of quercetin is depen-
dent on the form of quercetin that is ingested, with the gly-
coside forms of quercetin resulting in better absorption than
quercetin aglycone (21). However, studies found that both
forms are readily bioavailable (10,21–23). For example, we
found that a single 1095-mg dose of quercetin aglycone sup-
plement (24) and a 4-wk regimen of 730 mg quercetin/d
(10) can significantly increase plasma quercetin concentra-
tions 3-fold over baseline.
Other factors such as intestinal flora and dietary compo-
nents can affect the bioavailability of various isoforms of
quercetin. For example, supplementing pectin and rutin to-
gether results in increased quercetin plasma concentrations
in mice (25). Similar results were observed in rats fed a
diet high in pectin that were orally administered a single
50-mg/kg dose of quercetin (26), although enhancement
of absorption in this study was not attributed to alterations
in intestinal flora. Consumption of dietary fat was shown to
enhance absorption of both quercetin aglycone and querce-
tin-3-O-glycoside in pigs (27,28). Few studies examined the
ability of other polyphenolic compounds to influence quer-
cetin absorption; however, it was reported that cosupple-
mentation of epigallocatechin gallate and quercetin can
increase epigallocatechin gallate absorption in rats (29).
Apple, Red Delicious
Amount of quercetin in selected foods1
Quercetin content (mg/100 g)
1Adapted from USDA database (20).
40Larson et al.
All forms of quercetin (aglycone and quercetinwith glyco-
sides) are absorbed in the small intestine and colon. Studies
using rodents and humans indicate that quercetin glycosides
are hydrolyzed before absorption by a lactase phloridzin hy-
drolase enzyme before being absorbed as quercetin aglycone,
whereas quercetin aglycone is absorbed intact (30–34). Once
in the plasma, quercetin is bound to albumin (35) and trans-
ported to the liver (19). In the liver, quercetin (aglycone or
with glycosides) is rapidly converted to one or more metabo-
lites including isorhamnetin, kaempferol, and tamarixetin. In
our laboratory, we found high plasma concentrations of iso-
rhamnetin and, to a lesserextent,kaempferolin rats fed quer-
cetin-supplemented (0.15%) diets for 11 wk (36). Others
found isorhamnetin and tamarixetin in human plasma after
quercetin aglycone supplementation (22). These stable me-
tabolites of quercetin are also distributed throughout the
body tissues via albumin (37).
Quercetin is believed to be antimutagenic in vivo, and
long-term studies have not supported a carcinogenic role
for quercetin (38). Few negative side effects have been noted
with short-term (<3 mo), high intake of quercetin aglycone
(10,22,39), but there have been signs of nephrotoxicity (in-
creased serum creatinine) after large doses (w3600 mg)
were administered intravenously to patients being treated
for cancer (reviewed in 38]). Quercetin is also an inhibitor
of CYP3A4, an enzyme that breaks down many commonly
prescribed drugs in the body; therefore, quercetin should
not be taken with drugs that depend on this enzyme for me-
tabolism. Because many flavonoids were found to inhibit
platelet aggregation (via inhibition of thromboxane A2)
(40,41), it is also possible that pharmacological doses of
quercetin could increase the risk of bleeding when taken
with anticoagulant drugs.
Therapeutic role of quercetin to decrease blood pressure
in animals and humans
Please note that all studies reviewed here used the aglycone
form of quercetin (Fig. 1) unless otherwise noted. Quercetin
has been shown to have vasodilator effects in vitro using iso-
lated rat arteries (42–44). This vasodilatory effect is also ob-
served using metabolites of quercetin such as isorhamnetin,
tamarixetin, and kaempferoland is reported to be independent
Chemical structure of quercetin and its various forms.
Quercetin and hypertension41
of the endothelium (42,44). It should also be noted that the
vasodilatory effect of quercetin appears to be more pro-
nounced in resistance (e.g., mesenteric arteries) compared
with conductance (e.g., aorta) arteries (42,44). Given the
data obtained from these in vitro studies, it is not surprising
that a number of laboratories, including our own, have re-
ported that quercetin lowers blood pressure in spontane-
ously hypertensive (11,45) and Dahl salt-sensitive rats (46)
as well as rats that consume a high-fat, high-sucrose diet
(47), are deficient in NO (48), are infused with angiotensin
I (49), or have experimentally induced pressure overload us-
ing aortic constriction (12). The aforementioned animal
studies have provided important proof-of-principle that
quercetin may be efficacious in decreasing blood pressure
in humans with hypertension.
The antihypertensive effects of quercetin found in ani-
mals have also been reproduced in humans. The magnitude
of blood pressure reduction is often greater in animal stud-
ies, and one could speculate that this may be related to fac-
tors such as the dose used (greater in animal studies than in
human studies), and the severity of hypertension present in
the animal models. Nevertheless, it is noteworthy that across
models, quercetin has consistently been demonstrated to de-
crease blood pressure.
Supplementation of the diet with quercetin aglycone has
been shown to decrease blood pressure in hypertensive indi-
viduals, but not those with prehypertension or normal
blood pressure. For example, we conducted a randomized,
double-blind, placebo-controlled, crossover trial to investi-
gate the efficacy of quercetin supplements on stage 1 hyper-
tensive (140–159 mm Hg systolic and 90–99 mm Hg
diastolic, n = 22) and prehypertensive (20–139 mm Hg sys-
tolic and 80–89 mm Hg diastolic, n = 19) participants. De-
creases (P < 0.01) in systolic (27 6 2 mm Hg), diastolic
(25 6 2 mm Hg), and mean arterial blood pressure
(25 6 2 mm Hg) were observed in subjects with hyperten-
sion after supplementation with 730 mg/d of quercetin for
28 d vs. placebo. In our study, we did not find any change
in blood pressure in subjects with prehypertension (Fig.
2). Similar results have been observed in normotensive,
healthy humans supplemented daily with 1000 mg of quer-
cetin and 200 mg of rutin (quercetin-3-rutinoside) who
demonstrate a marked increase in plasma quercetin levels
after 4 wk, but no change in blood pressure (39). Likewise
we have observed that quercetin does not decrease blood
pressure in normotensive rodents, but only in hypertensive
In contrast to our work, 2 studies conducted by Egert
et al. (50,51) found that 150 mg/d of quercetin for 6 wk de-
creased blood pressure in overweight and obese prehyper-
tensive individuals. Both studies by Egert et al. found
statistically significant decreases in systolic pressure of w3
mm Hg; however, it was found that the effect was only pre-
sent in subjects that were homozygous for the apolipopro-
tein E3 genotype (51). Subjects carrying a copy of
apolipoprotein E4 did not have lower blood pressure after
quercetin supplementation (51). There are several possible
explanations for the discrepancies in the effect and magni-
tude of the decrease in blood pressure between our studies
and those of Egert et al. For example, the differences may
be related to the dose of quercetin used (150 vs. 730 mg/d),
the duration of supplementation (42 vs. 28 d), the genotype
of participants, and/or the sample size used (n = 93 vs. n =
19). However, all human studies to date are in broad agree-
ment that quercetin supplementation can decrease blood
pressure in hypertensive individuals.
Potential mechanisms for blood pressure reduction
Evidence exists to support several potential mechanisms
whereby quercetin might decrease blood pressure and de-
crease the severity of hypertension in animals and humans.
These mechanisms are a decrease in oxidative stress, interfer-
ence with the renin-angiotensin-aldosterone system (RAAS),
and /or improving vascular function in an endothelium-de-
pendent or -independent manner.
Quercetin and oxidative stress. Because oxidative stress has
been linked to impaired vasodilation and kidney function in
animal modelsofhypertension(52), many studies have exam-
ined the role of antioxidants to treat hypertension. Previous
studiesfound thatadecreasein blood pressure in hypertensive
animals and humans treated with quercetin is due to a de-
that treatment of spontaneously hypertensive rats with
changes observed after a double-blind,
placebo-controlled trial comparing 4 wk of 760
mg/d quercetin supplementation vs. placebo
in male and female patients with hypertension.
MAP, mean arterial pressure. Values are mean
6 SE, n = 22 stage 1 hypertensive, n = 19
Prehypertensive. *Different from placebo;
P , 0.05. Adapted with permission from (10).
Summary of blood pressure
42Larson et al.
aortic segments and decreased systolic blood pressure by 18%.
Because indices of oxidative stress (e.g., urinary F2 isoprostane
and plasma malondialdehyde) were lowered after quercetin
treatment, the improvement in endothelial function was at-
tributed to the antioxidant effect of quercetin. Other animal
studies have also found that decreases in blood pressure after
quercetin supplementation occur in conjunction with im-
proved indices of oxidative stress such as plasma lipid perox-
ides and urinary isoprostanes (marker of lipid peroxidation)
tioxidant effect of quercetin might have been the mechanism
for blood pressure reduction. However, not all animal studies
found that quercetin exerts a strong antioxidant effect. In our
laboratory, we found that quercetin-supplemented chow can
decrease blood pressure and hepatic malondialdehyde levels
in pressure-overloaded (12), but not spontaneously hyperten-
sive rats (36).
Similar to the equivocal findings in animals studies, hu-
man investigations using various quercetin doses have not
consistentlydemonstrated an antioxidant effect of quercetin.
Egert et al. (22) demonstrated that 150 mg of quercetin for 2
wk in healthy, normotensive individuals did not affect
plasma oxidized low-density lipoprotein, ferric-reducing an-
tioxidant potential, oxygen radical absorbance capacity, or
inflammatory markers, In a later study conducted by the
same group using 93 hypertensive individuals with symp-
toms of metabolic syndrome, 150 mg of quercetin for 6
wk was enough to decrease systolic blood pressure by 2.6
mm Hg (P < 0.05) and oxidized low-density lipoprotein,
but not inflammatory markers or plasma antioxidant capac-
ity (50). We found similar results that quercetin lowers sys-
tolic blood pressure by 7 mm Hg, but not indicators of
oxidant load (plasma antioxidant capacity or urinary iso-
prostane concentration) in hypertensive humans with met-
abolic syndrome (10).
Although a great dealofevidence obtained fromhyperten-
sive animal models indicates that quercetin might be effective
in decreasing oxidant load, available data from humans is
equivocal. In general, higher doses of quercetin have been
evaluated in animals compared with humans, and this may
lead to significant differences in the intracellular concentra-
tions of quercetin and subsequent antioxidant effects. In
hyde levels in rats fed quercetin-supplemented diets (150 mg/
kg of quercetin) (12), but not in hypertensive humans in
whom w8.1 mg quercetin/kg body weight failed to alter
plasma antioxidant power or urinary isoprostanes (10). One
key difference between these studies is the fact that plasma
quercetin levels were 3.96 mg/mL in rats, but only 0.48 mg/
mLinhumans (corresponding to a 2-fold increasefrombase-
line). This raises the possibility that the difference in plasma
quercetin concentrations was responsible for the disparate ef-
fects on oxidative stress. Because inconsistent evidence exists
for the ability of quercetin to act as an antioxidant in vivo, it
remains possible that the blood pressure–lowering effect of
quercetin may be due to other mechanisms.
Quercetin and RAAS. The RAAS (Fig. 3) plays a major role
in the regulation of blood pressure. There is a great deal of
evidence that long-term overactivation of this system leads
to hypertension and other CVDs (reviewed in ). The
use of ACE inhibitors or subtype-specific angiotensin recep-
tor blockers can interfere with the RAAS and lead to a de-
crease in both blood pressure and cardiovascular events in
high-risk populations (53,54). Quercetin has been shown
to inhibit ACE in vitro (55), presumably through its ability
to chelate metal ions such as zinc (43). Interestingly, the
mechanism of action by which ACE inhibitors such as cap-
topril and imidapril inhibit ACE is by binding a zinc atom at
the active site of the enzyme, which slows conversion of an-
giotensin I to angiotensin II (56). Häckl et al. (49) demon-
strated that both oral and intravenous administration of
quercetin in Wistar rats attenuates the increase in blood
pressure evoked by intravenous infusion of angiotensin I.
This study also reported a 31% decrease in ACE activity after
quercetin treatment compared with baseline (49),suggesting
that quercetin acted as an ACE inhibitor. Mackraj et al. (46)
also compared the long-term antihypertensive effects of cap-
topril with those of quercetin using Dahl salt-sensitive rats
that were given daily injections for 4 wk of captopril (ACE
inhibitor), quercetin, or vehicle. Although blood pressure
increased in vehicle-treated Dahl rats during the 4-wk pe-
riod, it was significantly decreased compared with baseline
in both quercetin- and captopril-treated groups. The de-
crease in blood pressure occurred in parallel with down-reg-
ulation of the angiotensin-I receptor in the kidney, increased
urine volume, and increased urinary sodium excretion (46),
thus providing a potential mechanism for the long-term
blood pressure–lowering effects of quercetin. Taken to-
gether, the aforementioned studies indicate that quercetin
may engage in multiple points in the RAAS to decrease
blood pressure (Fig. 3). Given the proven efficacy of phar-
macological ACE inhibition in humans and the animal-
based evidence suggesting quercetin may act as an ACE
inhibitor, there is a need to conduct clinical trials to deter-
mine whether quercetin supplementation can decrease
ACE activity in hypertensive humans.
Quercetin and vascular function. The innermost lining of
the blood vessel wall is composed of a single-cell layer–thick
structure called the endothelium. The endothelium plays a
very important role in maintaining vascular homeostasis, vas-
thelial dysfunction is a critical event in the pathogenesis of
CVD and an independent predictor of cardiovascular events
NO) or constrict (e.g., ET-1) the blood vessel, which thereby
regulates blood pressure and blood flow (58.59). A common
feature of endothelial dysfunction is decreased bioavailability
to circulating vasoconstrictors [e.g., ET-1 (4)]. NO and ET-1
appear to have a reciprocal regulation; as NO bioavailability
Quercetin and hypertension43
decreases, there is enhanced synthesis and/or response to ET-1
(59). Endothelial dysfunction is reversible, and interventions
that decrease the risk of CVD, such as exercise and pharma-
ceuticals, are associated with improved endothelial function;
it has become a surrogate biomarker for determining the ef-
ficacy of CVD interventions (59).
Quercetin decreased blood pressure in rodents that was
accompanied by improvements in endothelial function
(11,47,48). For example, Duarte et al. (11) reported that
spontaneously hypertensive rats given 10 mg quercetin/kg
body weight (via gavage) have improved endothelium-de-
pendent vasorelaxation in isolated aorta and decreased
blood pressure. Similar results have been found when quer-
cetin is administered to rats with hypertension that is pro-
duced by NO synthase inhibition (48). Using a dietary
model of hypertension (high-fat, high-sucrose diet for 4
wk), Yamamoto and Oue (47) observed hypertension, low
aortic NO synthase activity, and low urinary NO metabo-
lites, all of which were reversed by quercetin consumption.
Collectively, these studies provide evidence that one poten-
tial mechanism by which quercetin can decrease blood pres-
sure is through improved endothelial function evoked by
increased NO bioavailability and/or NO production.
Previous studies focused on determining whetherquerce-
tin improves vascular function due to NO-dependent mech-
anisms; however, findings of a recent study by Loke et al.
(60) suggest that decreased levels of ET-1 may also contrib-
ute to quercetin’s antihypertensive effect. In this study, the
acute effects of a single 200-mg dose of quercetin were ex-
amined in healthy, normotensive males. Although blood
pressure was not measured, it was reported that 2 h after
quercetin supplementation, plasma ET-1 was lower, and af-
ter 5 h, urinary metabolites of NO were higher with querce-
tin treatment compared with placebo treatment (60). Along
these lines, in vitro studies also found that quercetin can de-
crease ET-1 expression and release in human umbilical vein
endothelial cells in a dose-dependent manner (61,62). Even
though the study by Loke et al. was conducted in healthy
males rather than individuals with hypertension, the data in-
dicate that improving the balance between vasoconstrictors
(ET-1) and vasodilators (NO) may be another possible
mechanism by which quercetin could improve vascular
function and decrease blood pressure.
There is also evidence that quercetin may decrease blood
pressure through mechanisms independent of the endothe-
lium by directly acting on the vascular smooth muscle. In
this regard, both quercetin and isorhamnetin (a metabolite
of quercetin) can evoke vasorelaxation in the aorta and
smaller resistance arteries of rodents regardless of whether
the endothelial layer of vessels is intact or denuded
(42,44). Likewise, it has been reported that flow-mediated
vasodilation is improved in humans who consume querce-
tin-rich foods, but with no corresponding change in endo-
thelium-dependent function (41). It remains unclear how
quercetin evokes endothelium-independent relaxation, but
it has been speculated that it results from inhibition of
the renin-angiotensin-aldosterone system to decrease blood pressure, as reviewed in the text.
Overview of possible mechanisms based on available in vitro and in vivo evidence by which quercetin (Q) may interact with
44Larson et al.
protein kinases involved in the Ca2+-sensitizing mechanisms
responsible for smooth muscle contraction (44).
In vitro and in vivo research conducted using animal models
has shown multiple potential mechanisms of action that
could produce the blood pressure–lowering effect of querce-
tin seen in hypertensive humans. However, definitive evi-
dence of a precise mechanism of action by which quercetin
might decrease blood pressure in humans remains elusive.
In conjunction with discovering mechanisms of action,
more controlled, randomized human research studies are
needed to confirm quercetin’s efficacy, magnitude of effect,
and optimal dosing schedule. Furthermore, it needs to be de-
termined whether quercetin is an effective treatment for all
formsofhypertensionregardlessofpathological origin. How-
ever, despite the uncertainty of the mechanism of action of
quercetin in humans, this flavonoid has promise for the treat-
ment of hypertension and warrants larger scale clinical trials
than have been done to date.
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