Brief Review

Is There a Pathogenetic Role for Uric Acid in Hypertension

and Cardiovascular and Renal Disease?
Richard J. Johnson, Duk-Hee Kang, Daniel Feig, Salah Kivlighn, John Kanellis, Susumu Watanabe,
Katherine R. Tuttle, Bernardo Rodriguez-Iturbe, Jaime Herrera-Acosta, Marilda Mazzali

Abstract—Hyperuricemia is associated with hypertension, vascular disease, renal disease, and cardiovascular events. In
this report, we review the epidemiologic evidence and potential mechanisms for this association. We also summarize
experimental studies that demonstrate that uric acid is not inert but may have both beneficial functions (acting as an
antioxidant) as well as detrimental actions (to stimulate vascular smooth muscle cell proliferation and induce endothelial
dysfunction). A recently developed experimental model of mild hyperuricemia also provides the first provocative
evidence that uric acid may have a pathogenic role in the development of hypertension, vascular disease, and renal
disease. Thus, it is time to reevaluate the role of uric acid as a risk factor for cardiovascular disease and hypertension
and to design human studies to address this controversy. (Hypertension. 2003;41:1183-1190.)
Key Words: antioxidants 䡲 hypertension, essential 䡲 cardiovascular diseases 䡲 renin-angiotensin system
䡲 vascular diseases 䡲 renal disease

U ric acid, a product of purine metabolism, is degraded in

most mammals by the hepatic enzyme, urate oxidase
(uricase), to allantoin, which is freely excreted in the urine.
Hyperuricemia Is Increased in Subjects at
Cardiovascular Risk
Serum uric acid is frequently elevated in subjects at cardio-
However, during the Miocene epoch (20 to 5 million years vascular risk (Table 1).6 –15 Uric acid is higher in men and
ago), 2 parallel but distinct mutations occurred in early postmenopausal women because estrogen is uricosuric.8 In
hominoids that rendered the uricase gene nonfunctional.1 As subjects with obesity, insulin resistance, and dyslipidemia
a consequence, humans and the great apes have higher uric (“the metabolic syndrome”), hyperuricemia frequently occurs
acid levels (⬎2 mg/dL) compared with most mammals (⬍2 because insulin stimulates sodium and urate reabsorption in
mg/dL). the proximal tubule.8 Uric acid is increased in subjects with
Uric acid levels also vary significantly within humans as renal disease as the result of reduction in GFR and renal urate
the result of factors that increase generation (such as high excretion. Diuretics, such as thiazides, increase serum uric
purine or protein diets, alcohol consumption, conditions with acid by stimulating both sodium and urate reabsorption in the
high cell turnover, or enzymatic defects in purine metabo- proximal tubule. Alcohol intake results in elevated uric acid
lism) or decrease excretion. A reduction in glomerular filtra- levels due to increased urate generation (from increased
tion rate (GFR) increases serum uric acid, although a signif- adenine nucleotide turnover) and decreased excretion (due to
icant compensatory increase in gastrointestinal excretion lactate blocking tubular transport of urate).14,15
occurs.2 Hyperuricemia also may result from increased net Uric acid is also commonly associated with hypertension.
tubular absorption. After filtration, uric acid undergoes both It is present in 25% of untreated hypertensive subjects, in
reabsorption and secretion in the proximal tubule, and this 50% of subjects taking diuretics, and in ⬎75% of subjects
process is mediated by a urate/anion exchanger and a voltage- with malignant hypertension.9 The increase in serum uric acid
sensitive urate channel.3,4 Organic anions such as lactate in hypertension may be due to the decrease in renal blood
decrease urate secretion by competing for urate through the flow that accompanies the hypertensive state, since a low
organic anion transporter, whereas several substances, includ- renal blood flow will stimulate urate reabsorption.10 Hyper-
ing probenacid and benziodarone, have opposite effects.5 tension also results in microvascular disease, and this can lead
Hyperuricemia is usually defined as ⬎6.5 or 7.0 mg/dL in to local tissue ischemia.11 In addition to the release of lactate
men and ⬎6.0 mg/dL in women. that blocks urate secretion in the proximal tubule, ischemia

Received January 9, 2003; first decision January 30, 2003; revision accepted March 21, 2003.
From the Division of Nephrology (R.J.J., D.-H.K., J.K., S.W., M.M.) and Texas Children’s Hospital (D.F.), Baylor College of Medicine, Houston, Tex;
Merck and Company, Inc (S.K.), West Point, Pa; The Heart Institute of Spokane (K.R.T.), Spokane, Wash; Hospital Universitario and Universidad del
Zulia (B.R.-I.), Maracaibo, Venezuela; and Instituto de Cardiologia (J.H.-A.), Mexico City, Mexico.
Correspondence to Richard J. Johnson, Baylor College of Medicine, Division of Nephrology, SM-1273, 6550 Fannin St, Houston, TX 77030. E-mail
[email protected]
© 2003 American Heart Association, Inc.
Hypertension is available at http://www.hypertensionaha.org DOI: 10.1161/01.HYP.0000069700.62727.C5

1183
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1184 Hypertension June 2003

TABLE 1. Uric Acid Is Increased in Groups at Cardiovascular Risk

Group Mechanism
Postmenopausal women and men Estrogen is uricosuric6
African Americans7 Unknown
Renal disease Decrease in GFR increases uric acid levels
Diuretics Volume contraction promotes urate reabsorption
Obesity/insulin resistance Insulin increases sodium reabsorption and is tightly linked to urate reabsorption8
9
Hypertension Urate reabsorption increased in setting of increased renal vascular resistance;10 microvascular disease
predisposes to tissue ischemia that leads to increased urate generation (from adenosine breakdown)
and reduced excretion (due to lactate competing with urate transporter in the proximal tubule);11 some
hyperuricemic hypertension may be due to alcohol ingestion12 or lead intoxication13
Alcohol use Increases urate generation,14 decreases urate excretion15
GFR indicates glomerular filtration rate.

also results in increased uric acid synthesis.16 With ischemia, antioxidants in plasma.57–59 Urate (the soluble form of uric
ATP is degraded to adenine and xanthine, and there is also acid in the blood) can scavenge superoxide, hydroxyl radical,
increased generation of xanthine oxidase. The increased and singlet oxygen and can chelate transition metals.57–59
availability of substrate (xanthine) and enzyme (xanthine Peroxynitrite is a particularly toxic product formed by the
oxidase) results in increased uric acid generation as well as reaction of superoxide anion with nitric oxide that can injure
oxidant (O2⫺) formation. The finding that ischemia results in cells by nitrosylating the tyrosine residues (nitrotyrosine
an increase in uric acid levels may also account for why uric formation) of proteins. Uric acid can also block this
acid is increased in preeclampsia17 and congestive heart reaction.60
failure.18 Other factors may also contribute to why uric acid Recently, Hink et al61 reported that uric acid may also
is associated with hypertension, including alcohol abuse,12 prevent the degradation of extracellular superoxide dismutase
lead intoxication,13 obesity and insulin resistance,8 and di- (SOD3), an enzyme critical in maintaining endothelial and
uretic use. vascular function. SOD3 is an extracellular enzyme that
The observation that an elevated uric acid is associated catalyzes the reaction of superoxide anion (O2⫺䡠) to hydrogen
peroxide (H2O2). The removal of O2⫺䡠 by SOD3 prevents the
with subjects at cardiovascular risk may account for why
reaction and inactivation by O2⫺䡠 of the important endothelial
hyperuricemia predicts the development of cardiovascular
vasodilator, nitric oxide (NO). SOD3, by removing O2⫺䡠,
disease in the general population (Table 2), in subjects with
therefore helps to maintain NO levels and maintain endothe-
hypertension (Table 3), and in subjects with preexisting
lial function.
cardiovascular disease (Table 4).19 – 47 Hyperuricemia also
Normally, SOD3 is inactivated in the presence of H2O2,
predicts stroke in diabetic and nondiabetic subjects48,49 and suggesting a feedback inactivation of the enzyme. However, uric
predicts the development of hypertension50 –52 and renal acid blocks SOD inactivation by H2O2 by regenerating SOD3
disease in the general population.53 In these studies, uric acid with the production of a urate radical.61 This latter radical,
may be simply “marking” subjects at increased cardiovascu- although potentially a pro-oxidant, has been found to be mark-
lar and renal risk.54,55 Consistent with this hypothesis, many edly less reactive than classic oxidants and can be rapidly
studies have found that uric acid is not an independent risk regenerated back to urate in the presence of ascorbate.62
factor for cardiovascular disease after controlling for these Ames et al57 hypothesized that the uricase mutation
other risk factors (Tables 2 through 4). Hyperuricemia is occurred during early hominoid evolution because the
therefore considered benign unless associated with gout or antioxidant action of uric may have provided an evolution-
kidney stones.56 ary advantage and that this may account for the greater
Nevertheless, some studies find uric acid predictive for the longevity of humans and the great apes compared with
development of cardiovascular disease, hypertension, and most other primates. The increase in serum uric acid in
renal disease despite controlling for associated risk factors. subjects with cardiovascular disease might therefore re-
This raises the possibility that uric acid may have a patho- flect a compensatory mechanism to counter the oxidative
genic role in hypertension and cardiovascular disease. Indeed, stress that occurs in these conditions.63 However, this does
recently soluble uric acid has been recognized to not be inert not readily explain why higher uric acid levels in patients
but rather to have several biological actions that could either with cardiovascular disease are generally associated with
be beneficial or detrimental to humans. We now review these worse outcomes (Tables 3 and 4).
studies and provide an interpretation for how they may relate
to human disease. Is Uric Acid a Mediator of Hypertension and
Renal Disease?
Uric Acid as an Antioxidant: A Protective Uric Acid, Endothelial Dysfunction, and Impaired
Factor in Cardiovascular Disease? Nitric Oxide Production
An important observation was that uric acid may function as Endothelial dysfunction, local oxidant generation, elevated
an antioxidant, and possibly one of the most important circulating cytokines, and a proinflammatory state are com-
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 Johnson et al Uric Acid, Hypertension, and Renal Disease 1185

TABLE 2. Hyperuricemia Predicts Cardiovascular Events: Studies of the

General Population
Length of Univariate Independent Predictor
Follow-Up, Correlation in Multivariate
Study y With Events Analyses
Framingham
198519 26 Yes No
198720 30 Yes Yes (women)
198821 32* Yes Yes
199922 17.3† Only women No
Honolulu Heart (Japanese American men)
197523 2 Yes Yes
24
1995 20 Yes Yes
199625 21 Yes Yes
(in alcohol abstainers)
Chicago Heart Association Detection Project
197926 5 Yes Yes (only women)
198927 11.5 Only women Yes (only women)‡
NHANES I
199528 13.5 Yes Yes (only women)
200029 16.4 Yes Yes
ARIC (Atherosclerosis Risk in Communities
Study)
200030 8 Only women No
British Regional Heart Study (adult males)
199731 16.8 Yes No
Social Institute of Finland
198232 5 Yes No
Gothenburg
198833 12 Yes Yes‡
MONICA (Monitoring Trends and Determinants
in Cardiovascular Diseases)
199934 8 Yes Yes‡
CASTEL (Cardiovascular Study in the Elderly)
199335 7 Yes Yes‡
*Subanalysis of men with gout.
‡For all-cause mortality.
†Includes original participants of the Framingham Study who took part in the 13th biennial exam
and participants of the Framingham Offspring Study.

mon in patients with cardiovascular disease.18,64 Endothelial after coronary artery bypass68 –70 and in patients with dilated
dysfunction is often demonstrated by showing an impaired cardiomyopathy.71 Although the beneficial effects correlate
NO release in response to acetylcholine, which results in with the lowering of uric acid in some of these studies, most
impaired endothelium-dependent vasodilation. Oxidants may authorities have hypothesized that the beneficial effect of
cause endothelial dysfunction by reacting with and removing allopurinol is to reduce oxidative stress.65–70
the NO. The observation that xanthine oxidase generates Uric acid may contribute to endothelial dysfunction. Waring et
oxidants and uric acid in settings of tissue ischemia poten- al72 have reported that uric acid infusion in healthy humans resulted
tially explains why uric acid is associated with endothelial in impaired acetylcholine-induced vasodilation in the forearm,
dysfunction and oxidative stress in conditions such as heart thereby documenting impaired endothelial NO release. Serum uric
failure and diabetes.65– 67 Hyperuricemia is also associated acid and serum nitric oxide levels also vary during the day in a
with the activation of circulating platelets, which also may reciprocal pattern, suggesting a pattern of physiological regulation.73
reflect endothelial dysfunction.68 Allopurinol, which inhibits Recent studies in experimental animal models have also found that
xanthine oxidase and hence blocks both uric acid and oxidant mild hyperuricemia inhibits the nitric oxide system in the kidney
formation, can reverse the impaired endothelial NO produc- (see below).
tion in both heart failure and type 2 diabetes.65– 67 Allopurinol The mechanism by which uric acid impairs endothelial
has also been reported to reduce cardiovascular complications function is not known. However, whereas uric acid is con-
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1186 Hypertension June 2003

TABLE 3. Hyperuricemia Predicts Cardiovascular Events: Studies of the Hypertensive Population

Length of Univariate Independent Predictor
Follow-Up, Correlation in Multivariate
Study y with Events Analyses
Hypertension Detection Follow-Up Program
Cooperative Research Group
198536 5 Yes Yes
198737 5† Yes Only women
Work site
199938 6.6 Yes Yes
PIUMA (Progetto Ipertensione Umbria
Monitoraggio Ambulatoriale)
200039 4 Yes Yes
European Working Party on High BP in the Elderly
199140 3 Yes No
SHEP (Systolic Hypertension in the Elderly
Program)*
200141 5 Yes Yes
Syst-China*
200142 3 Yes Yes
Syst-Eur*
200243 2 No No
*Patients with isolated systolic hypertension; †subanalysis of patients on thiazides.

sidered an antioxidant, it is also pro-oxidative under certain and AP-1.81 MCP-1 is a chemokine that is important in
conditions, especially when other antioxidants are at a low vascular disease and atherosclerosis.82 Soluble uric acid also
level.74,75 stimulates human mononuclear cells to produce interleukin-
1␤, interleukin-6, and tumor necrosis factor (TNF)-␣.83 Infu-
Uric Acid, Vascular Smooth Muscle Cell sion of uric acid into mice also leads to a marked increase in
Proliferation, and Inflammation circulating TNF-␣ levels.84 Thus, in experimental and in vitro
Uric acid also stimulates rat vascular smooth muscle cell systems, uric acid appears to have the ability to induce
proliferation in vitro.76 –79 Vascular smooth muscle cells do inflammatory and vascular mechanisms that may contribute
not express a receptor for uric acid but rather have organic to rather than protect against the development of cardiovas-
anion transporters that allow urate uptake.80 Once inside the cular disease.
vascular smooth muscle cell, uric acid activates specific
mitogen activated protein kinases (Erk1/2) with the de novo Experimental Models: Hypertension in
induction of cyclooxygenase-2 (COX-2), local thromboxane Hyperuricemic Rats
formation, and with upregulation of platelet-derived growth Recently, mild hyperuricemia was developed in rats through
factor A (PDGF A) and C-chain and PDGF-␣ receptor the use of a uricase inhibitor (oxonic acid). Unlike previous
mRNA76 –79 (Figure). The uric acid–induced cell proliferation hyperuricemic models,85,86 this model was associated with no
can be inhibited by blocking any member of this urate crystal deposition in the kidney and relatively preserved
pathway.76 –79 renal function.87 A remarkable observation, now documented
Soluble uric acid also is proinflammatory. Uric acid by two different laboratories, was that systemic hypertension
stimulates synthesis of monocyte chemoattractant protein-1 developed in hyperuricemic rats after several weeks.77,78,87,88
(MCP-1) in rat vascular smooth muscle cells by activating The hypertension was associated with increased renin and a
p38 MAP kinase and the nuclear transcription factors, NF-␬B decreased neuronal nitric oxide synthase (NOS1) in the

TABLE 4. Hyperuricemia Predicts Cardiovascular Events in Patients With

Pre-Existing Cardiovascular Disease
Univariate Independent Predictor
Correlation in Multivariate
Study With Events Analyses
Coronary Drug Project Research Group, 197644 Yes No
French Canadian Study, 197345 No Not done
Atherogene Study, 200246 Yes Yes
The Heart Institute of Spokane, 200247 Yes Yes

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 Johnson et al Uric Acid, Hypertension, and Renal Disease 1187

TABLE 5. Hyperuricemia Predicts the Development

of Hypertension
Israeli Ischemic Heart Study, 197250
Kaiser Permanente Medical Care Program, 199051*
Olivetti Heart Study, 199452*
*Shown to independently predict the development of hypertension.

merular hypertrophy, and eventually, glomerulosclerosis and

albuminuria.90 Micropuncture studies document that this is
associated with an increase in glomerular hydrostatic pres-
sure.88 The renal changes are prevented if serum uric acid is
Pathway for uric acid–mediated vascular smooth muscle cell maintained in the normal range with allopurinol .88,90
proliferation. Uric acid is posited to enter into vascular smooth
muscle cell through an anion exchanger/transporter (OAT), Experimental hyperuricemia also accelerated injury in
where it alters intracellular redox, activates mitogen activated established models of renal disease. Hyperuricemia exacer-
protein kinases (Erk1/2 and p38), COX-2, and nuclear transcrip- bates cyclosporine nephropathy in rats, resulting in worse
tion factors (NF␬B and AP-1), leading to synthesis of
thromboxane (TXA2), PDGF and PDGF receptors, and MCP-1. tubulo-interstitial injury and arteriolar hyalinosis with in-
creased renin and a greater loss of macula densa NOS1 and
juxtaglomerular apparatus.87 The hypertension was prevented renal NOS3 expression.91 Hyperuricemia also accelerated
by administration of an ACE inhibitor and to a lesser extent progression in the remnant kidney model and resulted in
by L-arginine (a substrate for nitric oxide), thereby confirm- higher blood pressure, more proteinuria, worse renal function,
ing a key role for renin-angiotensin and NOS systems in the and more glomerulosclerosis and tubulo-interstitial fibrosis.79
blood pressure elevation. The hypertension and changes in These rats also had severe vasculopathy, involving the
renin and NOS1 were also prevented by maintaining uric acid interlobular artery and afferent arteriole with de novo expres-
levels in the normal range with allopurinol or benziodarone (a sion of COX-2 in the blood vessels and increased renal renin
uricosuric).87 expression. The renal changes were significantly improved by
Hyperuricemic rats were also shown to have salt sensitivity reducing uric acid levels with allopurinol.
(that is, a greater increase in blood pressure for the same
sodium load compared with normal rats).78 An explanation Do the Experimental Studies Provide
for the mechanism comes from studies in other experimental New Insights?
models that have shown that salt sensitivity may result from The observation that hyperuricemic animals have salt sensi-
preglomerular vascular disease.89 Experimental models asso- tivity and increased blood pressure provide an additional
ciated with preglomerular vascular disease have renal ische- mechanism to explain why the uricase mutation occurred in
mia, leading to the infiltration of leukocytes into the intersti- early hominoid evolution. Thus, the uricase mutation may
tium that generate local oxidants, altering the balance of local have provided an evolutionary advantage to early hominoids
vasoregulatory factors favoring vasoconstriction, and result- by maintaining blood pressure under the low sodium dietary
ing in a reduction in sodium excretion, a shift in pressure conditions of that period.78
natriuresis, and an increase in blood pressure. Elements of The observation that experimental hyperuricemia causes
this pathway have been demonstrated in a variety of animal hypertension, intrarenal vascular disease, renal disease, and
models, and the salt sensitivity can be prevented or amelio- vascular inflammation in rats may also provide the long-
rated by interrupting this pathway.89 sought pathogenic mechanism by which uric acid could cause
Consistent with this pathway of salt sensitivity, chronically cardiovascular disease in humans.
hyperuricemic rats have thickening and hypercellularity of Is there evidence that uric acid causes hypertension in
the afferent arteriole of the glomerulus, with inward hyper- humans? Epidemiological studies show a continuous relation
trophic vascular remodeling, leading to an increase in medial of serum uric acid with blood pressure that is stronger in
thickness and a reduction in lumen diameter.78 The arteriol- younger subjects with some dampening over time,19,20,92
opathy occurs independent of blood pressure, although it is which is consistent with the experimental studies that dem-
dependent on the renin-angiotensin system.77 In concert with onstrate that once sufficient renal injury occurs that animals
the development of preglomerular vascular disease, rats develop salt-sensitive hypertension regardless of the uric acid
manifest subtle tubulointerstitial inflammation and fibrosis.78 levels.78 Hyperuricemia is also an independent risk factor for
Once these renal changes develop, salt sensitivity can be predicting the development of hypertension (Table 5).51,52 To
shown. At this point, the kidney is driving salt sensitivity date, no studies have examined whether lowering uric acid
because correction of the elevated uric acid level is no longer will reduce blood pressure in hypertensive humans, but it
protective.78 should be noted that the above studies suggest that lowering
uric acid would be more effective at preventing rather than
Experimental Hyperuricemia and Renal Injury treating hypertension, for once the intrarenal vascular disease
Renal injury also occurs in hyperuricemic rats, consisting of develops, the hypertension would then be expected to be
afferent arteriolopathy, mild tubulointerstitial fibrosis, glo- driven by the kidney. Hyperuricemia also correlates with
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1188 Hypertension June 2003

plasma renin activity,93,94 and renal renin expression is also partially counter its potential detrimental effects. It is of
increased in hyperuricemic rats.87 interest that almost all studies examining the relation of
Does uric acid cause renal disease in humans? Patients uric acid levels with cardiovascular events show a
with gout frequently have renal dysfunction (25% to 40% of J-shaped curve with the nadir of risk being in the second
cases), with histologic injury in the majority.95 The renal quartile.20 –25,28,29,39,43,44 Although speculative, it is possi-
lesion consists of variable degrees of arteriolosclerosis, glo- ble that the increased risk for the lowest quartile reflects
merulosclerosis, and interstitial fibrosis, often with focal the decreased plasma antioxidant activity, whereas the
deposition of urate crystals in the outer medulla.95 Many increased risk at higher levels reflects the role of uric acid
authorities have ascribed the renal lesion to coexistent hyper- in inducing vascular disease and hypertension.
tension or aging-associated renal disease.96 However, this In conclusion, recent evidence supports a role for uric acid
type of analysis cannot account for all of the renal injury as a true cardiovascular risk factor, particularly for the
observed.97 development of hypertension and renal disease. Studies need
Recently, an elevated uric acid has been reported to predict to be performed in humans to prove or disprove this possi-
the development of renal insufficiency in individuals with bility before lowering uric acid is routinely recommended.
normal renal function.55 Uric acid is an independent predictor Given that hyperuricemia causes preglomerular vascular dis-
for progression in IgA nephropathy.98,99 Hyperuricemia also ease in rats, one might posit that it may be easier to show a
correlates with the development of renal dysfunction in type role for uric acid in hypertension by designing preventive
II diabetes100 and independently predicts progression in renal trials as opposed to treatment trials. However, it is possible
transplant patients on cyclosporine (Al-Uzri AY, Prather JC, that treating hyperuricemia may be effective in lowering
Norman DJ, Gloconda S, and de Mattos AM. Hyperuricemia blood pressure when the hyperuricemia has not been present
as a risk factor for renal allograft loss, American Transplant for a long period (such as in children with hypertension and
Congress, 2002, abstract). In contrast, it remains unclear if in patients given short-term treatment with cyclosporine or
uric acid is a risk factor for progression in subjects with diuretics) or when subjects are given a low salt diet (which
established renal disease. Although experimental studies would remove the renal injury– dependent mechanism).
suggest uric acid may act as a risk factor for progression,79 in
the MDRD study, uric acid was not found to be a risk Acknowledgments
factor.101 Furthermore, whereas some studies report an im- This study was supported by National Institutes of Health grants
provement in renal function with the lowering of uric acid in HL-68607, DK-52121, and 1P50DK-064233-01. Dr Mazzali is
gouty subjects,102,103 others have not been able to confirm supported by a postdoctoral grant from FAPESP-Fundação de
Amparo a Pesquisa do Estado de S. Paulo, Brazil.
these findings.104
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Is There a Pathogenetic Role for Uric Acid in Hypertension and Cardiovascular and Renal
Disease?
Richard J. Johnson, Duk-Hee Kang, Daniel Feig, Salah Kivlighn, John Kanellis, Susumu
Watanabe, Katherine R. Tuttle, Bernardo Rodriguez-Iturbe, Jaime Herrera-Acosta and Marilda
Mazzali

Hypertension. 2003;41:1183-1190; originally published online April 21, 2003;

doi: 10.1161/01.HYP.0000069700.62727.C5
Hypertension is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
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