original contributions
nature publishing group
Vasodilator Effects of Red Wines in Subcutaneous
Small Resistance Artery of Patients With Essential
Hypertension
Enzo Porteri1, Damiano Rizzoni1, Carolina De Ciuceis1, Gianluca E.M. Boari1, Caterina Platto1, Annamaria Pilu1,
Marco Miclini1, Claudia Agabiti Rosei1, Giuseppe Bulgari1 and Enrico Agabiti Rosei1
Background
It has been suggested that in animal models, red wine may have a
protective effect on the vascular endothelium. However, it is not
known whether this effect is also present in human small vessels and
whether it is specific for certain wines. The objective of this study is
to compare the vasodilator effects in subcutaneous small resistance
arteries of wines with different flavonoid content as well as of ethanol
vs. wines in normotensive (NT) subjects and in patients with essential
hypertension (EH).
Methods
Twenty-six EH and 27 NT were included in the study. Subcutaneous
small resistance arteries were dissected and mounted on a
micromyograph. Then we evaluated vasodilator responses as
concentration–response curves (20, 30, and 50 µl) to the following
items: (i) a red wine produced in small oak barrels (“en barrique”: EB)
(Barolo Oberto 1994), (ii) a red wine produced in large wood barrels
(LB) (Barolo Scarzello 1989), (iii) a red wine produced in steel tanks
Epidemiological studies have shown an association between
a moderate consumption of alcoholic beverage and a lower
incidence of cardiovascular events.1–3 Wine is the beverage
typically associated with cardioprotection, being presumably
a determinant of the low incidence of coronary heart disease
in France, the so-called French paradox.1 The epidemiological evidence comes along with the demonstration of beneficial
effects of alcohol or other wine products on some mediators
of cardiovascular disease, such as blood lipoproteins, clotting
and fibrinolytic factors, insulin sensitivity, endothelin, nitric
oxide (NO), and low-density lipoprotein susceptibility to oxidation.1 In particular, some polyphenolic components of red
wines, such as resveratrol, quercetin, or tannic acid, were demonstrated to possess vasoprotective properties.4–8 In particular, wine polyphenols may induce vasodilation by increased
1Clinica Medica, Department of Medical and Surgical Sciences, University of
Brescia, Brescia, Italy. Correspondence: Damiano Rizzoni ([email protected])
Received 11 September 2009; first decision 30 October 2009;
accepted 22 December 2009; advance online publication 21 January 2010.
doi:10.1038/ajh.2009.280
© 2010 American Journal of Hypertension, Ltd.
(Albarello Rosso del Salento 1997), and (iv) a white wine produced
in steel tanks in the presence or absence of an inhibitor of the nitric
oxide (NO) synthase (L-NMMA 100 µmol/l).
Results
A dose-dependent vasodilator effect of red wines (particularly EB and
LB) was detected in both NT and HT. The observed response was not
reduced after preincubation with L-NMMA.
Conclusions
Our results suggest red wines are more potent vasodilator than
ethanol alone, possibly depending on the content of polyphenols or
tannic acid. HT show similar responses compared with NT, indicating
that red wine is not harmful in this population.
Keywords: alcohol; blood pressure; endothelial function; flavonoids;
hypertension; polyphenols; red wine
Am J Hypertens 2010; 23:373-378 © 2010 American Journal of Hypertension, Ltd.
NO bioactivity.5,6,9 However, the previously mentioned data
have been obtained mainly in animal models or in cell cultures, although also in humans, some experimental evidence
supports an improvement of endothelial function after red
wine intake.8,10–12 However, comparison of postprandial studies and clinical trials concerning red wine consumption leads
to controversial results about its effect on endothelial function
and especially on flow-mediated vasodilation.13
It was also suggested that endothelium-dependent vasodilatory effects of red wines on rat aortic rings appear to be specific
for red “en barrique” wines, possibly because of their high content of phenolic substances.14 Although some study compared
standard vs. dealcoholized wine, it is not completely clear
whether the most active component of alcoholic beverages is
alcohol itself, or additional beneficial effects are provided by
polyphenols.1,10,15 In any case, possible endothelial-protective
properties of red wine might be of valuable clinical interest
because endothelial function in humans was demonstrated to
be a powerful predictor of cardiovascular events.16,17
In small arteries (<350 µm of lumen diameter), the endothelium seems to exert a key role in mediating vasoconstriction
AMERICAN JOURNAL OF HYPERTENSION | VOLUME 23 NUMBER 4 | 373-378 | april 2010
373
original contributions
and vasodilation.18 In addition, compounds produced by
endothelial cells may influence small resistance artery structure. Therefore, endothelial dysfunction and damage may
theoretically have an impact on vascular smooth muscle cells
and intercellular matrix proteins, and, hence, on small artery
remodeling. We have previously demonstrated that small
resistance artery structure is a powerful predictor of cardiovascular events in a high-risk population.19 It has also been
demonstrated that endothelial dysfunction may be observed
in several cardiovascular diseases, including hypertension. In
particular, the development of essential hypertension (EH) in
humans is usually associated with the presence of endothelial
dysfunction in small resistance arteries.20–22
Given all these considerations, we aimed to compare the
vasodilator effects in subcutaneous small resistance arteries of
wines with different flavonoid content as well as of ethanol vs.
wines in normotensive (NT) subjects and in patients with EH,
using a precise and reliable micromyographic technique.21,22
Methods
Twenty-six NT subjects and 27 patients with EH were included
in the study. Their age range was 38–67 years. The presence of hypertension was established according to European
Society of Hypertension/European Society of Cardiology
Guidelines.23 All hypertensive patients had been previously
treated for short periods of time with calcium channel blockers, angiotensin-converting enzyme inhibitors, diuretics, or
β-blockers. Treatment was withdrawn at least 3 weeks before
the procedure. The subjects and patients abstain from wine/
alcohol intake on the day of the experiment.
Venous blood samples were taken with the participants in
the supine position, after a therapeutic wash-out period of at
least 2 weeks, for standard hematology and serum biochemistry tests (including triglycerides and total cholesterol).
Micromyography. All subjects were then submitted to a biopsy
of subcutaneous fat from the gluteal or the anterior abdominal
region (3 cm long, 0.5 cm wide, and 1.5 cm deep). The biopsy
of the abdominal subcutaneous fat was taken during a surgical
procedure (usually cholecystectomy), whereas in the remaining cases, a standard skin biopsy of the gluteal region was
performed.21,22,24 Small arteries (about 100–280 μm of average diameter in relaxed conditions, 2 mm long) were dissected
from the subcutaneous fat of the biopsies and mounted as a
ring preparation on an isometric myograph (410 A; Danish
Myo Technology, Aarhus, Denmark) by threading onto two
stainless steel wires (40 μm diameter). The media-to-lumen
ratio of blood vessels in normalized condition was measured.
Details about the micromyographic technique of evaluation of
small artery morphology were previously reported.21,22
The vessels were then stimulated as follows:
Three stimulations (2 min for each) with physiological
saline solution in which NaCl was substituted with KCl
on an equimolar basis (K-PSS), and two stimulations with
K-PSS containing 10 μmol/l norepinephrine. If the wall
374
Vascular Function and Red Wines
tension developed during stimulation was >1 mN/mm,
then endothelial function was evaluated.
A cumulative concentration–response curve to acetylcholine at the following concentrations: 10−9, 10−8, 10−7,
10−6, and 10−5 mol/l, 3 min per concentration, after precontraction with norepinephrine 10 μmol/l (endotheliumdependent vasodilation).
A cumulative concentration–response curve to sodium
nitroprusside at the following concentrations 10−9,
10−8, 10−7, 10−6, and 10−5 mol/l, 3 min per concentration, after precontraction with norepinephrine 10 μmol/l
(­endothelium-independent vasodilation).
In addition, the vasodilation produced by different wines
was tested as concentration–response curve (20, 30, and 50 µl)
to the following:
1.A red wine produced in small oak barrels (“en barrique”:
EB) (Barolo Oberto 1994, Cuneo, Italy),
2.A red wine produced in large wood barrels (LB) (Barolo
Scarzello 1989, Cuneo, Italy),
3.A red wine produced in steel tanks (RST) (Albarello Rosso
del Salento 1997, Lecce, Italy), and
4.White wine produced in steel tanks (WST), (Breganze
Bianco 1996, Vicenza, Italy)
Vasodilator responses to different wines were evaluated after
precontraction with 10 μmol/l norepinephrine, in the presence or absence of L-NG-monomethylarginine (L-NMMA
100 µmol/l), an inhibitor of the NO synthase.
Finally, the direct vasodilator effects of ethanol (12%
­solution, same amount contained in the different wines) were
evaluated. The sequence of stimulations with wines/ethanol
was randomized.
Vasodilator responses were expressed as the percent decrease
of the wall tension (active force divided by two times the segment length) obtained with norepinephrine precontraction.
If the vessels produced rhythmic activity, the response was
measured from the mean active force for the last 20 s of each
period. All chemicals were dissolved in PSS, except sodium
nitroprusside (dissolved in glucose solution and protected
from light by aluminum foil). All drugs were obtained from
Sigma (St Louis, MO). Functional results from two different
blood vessels in each subject were averaged to provide one
mean observation per subject. For further details, see also
refs. 24,25. The protocol of the study was approved by the ethics committee of our institution (Medical School, University
of Brescia), and informed consent was obtained from each
participant. The procedures followed were in accordance with
institutional guidelines.
Statistical analysis. All data are expressed as mean ± s.d.
Comparison of continuous variables in the clinical study was
performed by Student’s t-test. One-way or two-way analysis
of variance was used to evaluate differences among groups,
when appropriate. The statistical significance was set at the
april 2010 | VOLUME 23 NUMBER 4 | AMERICAN JOURNAL OF HYPERTENSION
original contributions
Vascular Function and Red Wines
c­ onventional level of 5%. All analyses were carried out with
the BMDP statistical package (BMDP software programs 7D,
8D, 1V, and 2V; BMDP Statistical Software, Los Angeles, CA).
Results
Demographic data
The demographic, hemodynamic, and humoral data are
reported in Table 1. As expected, systolic and diastolic blood
pressures were significantly greater in essential hypertensives than in NT subjects. Fasting glucose, serum cholesterol,
serum triglycerides, and body mass index were similar in the
two groups of subjects. No signs of renal impairment were
observed, in terms of serum creatinine levels or calculated
glomerular filtration rate (data not shown).
Functional responses of subcutaneous small arteries
The vasodilator response to acetylcholine was greater in
NT subjects compared with essential hypertensive patients
Table 1 | Demographic, hemodynamic, and humoral data of the
study population
Parameter
Normotensive
subjects
(n = 26)
Essential
hypertensives
(n = 27)
Age (years)
54 ± 11.7
55 ± 4.9
Gender (M/F)
12M, 14F
12M, 15F
Body mass index
24.8 ± 0.91
26.1 ± 1.2
Fasting glucose (mmol/l)
5.54 ± 0.63
5.69 ± 0.72
Serum nitrogen (mmol/l)
13.0 ± 3.72
13.7 ± 1.77
Serum creatinine (µmol/l)
81.2 ± 12.6
84.1 ± 10.6
Cholesterol (mmol/l)
5.05 ± 1.23
5.46 ± 0.99
Triglycerides (mmol/l)
1.46 ± 0.57
1.60 ± 0.60
Systolic blood pressure (mm Hg)
125 ± 7.2
159 ± 7.5***
Diastolic blood pressure (mm Hg)
78 ± 5.3
99 ± 6.7***
***P < 0.001 vs. normotensives.
a
(­analysis of variance P < 0.001 between curves) (Figure 1),
whereas no difference was observed in vasodilator responses
to sodium nitroprusside (Figure 1).
Precontraction with norepinephrine was similar in vessels
from NT subjects and hypertensive patients (wall tension:
1.92 ± 0.43 vs. 2.22 ± 0.34, respectively, P = NS).
A dose-dependent vasodilator effect of red and white
wines was detected in both NT subjects and in hypertensive patients (Figure 2, Table 2). However, the vasodilator
response was clearly more evident with EB and LB compared
with WST and alcohol alone, whereas RST induced a vasodilator response intermediate between EB/LB and WST/alcohol alone (Figure 2, Table 2). The vasodilation observed with
EB and LB involved mainly non-NO-mediated mechanisms
because it was not significantly reduced after preincubation
with L-NMMA (Table 2). Finally, we observed a very modest
vasodilator effect with alcohol alone (Figure 2, Table 2), thus
suggesting that additional properties were possessed especially
by EB and LB.
Discussion
There are several epidemiological studies suggesting that
­moderate daily consumption of red wine may reduce cardiovascular risk,1–3,26 although it is not completely clear whether
red wines are superior to other sources of alcohol (beer, spirits). Results from a great number of mainly in vitro studies
indicate that constituents found in red wine are responsible for
some beneficial effects on endothelial cells.4–8,27,28 For the first
time, this study has evaluated direct effects of different wines
on small artery function in humans, using a direct, reliable, and
well-assessed technique. The main result of our study is that,
both in hypertensive patients and in NT subjects, a relevant
vasodilator effect may be observed after addition to the organ
bath of red wines produced in small oak barrels or in large
wood barrels, whereas a less pronounced effect was observed
with red wines produced in steel tanks. A very modest, almost
negligible effect was observed with white wine produced in
b
0
0
Hypertensives
−20
−40
−60
ANOVA P < 0.001
−80
−100
10−10
10−9
10−8
10−7
mol/l
10−6
10−5
10−4
% Reduction in wall tension
% Reduction in wall tension
Normotensives
Normotensives
Hypertensives
−20
−40
−60
−80
−100
10−10
10−9
10−8
10−7
mol/l
10−6
10−5
10−4
Figure 1 | Concentration-response curves to acetylcholine and sodium nitroprusside. (a) Endothelium-dependent vasodilation of subcutaneous small resistance
arteries (reduction of wall tension of subcutaneous small arteries after precontraction with norepinephrine and addition of acetylcholine). ANOVA P < 0.001
between normotensives (n = 27) and hypertensives (n = 26). (b) Endothelium-independent vasodilation of subcutaneous small resistance arteries (reduction
of wall tension of subcutaneous small arteries after precontraction with norepinephrine and addition of sodium nitroprusside). ANOVA P = NS between
normotensives and hypertensives. Data are mean ± s.e.m. ANOVA, analysis of variance; NS, not specified.
AMERICAN JOURNAL OF HYPERTENSION | VOLUME 23 NUMBER 4 | april 2010
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original contributions
a
% Vasodilatation
0
% Vasodilatation
% Vasodilatation
50 µl
0
Volume added to the bath
25 µl
30 µl
50 µl
EB
LB
RST
WST
Alcohol
−20
−40
0
Volume added to the bath
25 µl
30 µl
50 µl
EB
LB
RST
WST
Alcohol
−20
−40
−60
Table 2 | Vascular responses to wine/ethanol in the study
population (27 normotensives, 26 hypertensives)
EB
LB
RST
WST
Alcohol
−40
−60
c
30 µl
−20
−60
b
25 µl
Vascular Function and Red Wines
Volume added to the bath
Figure 2 | Vasodilator responses to various wines and alcohol. (a) Vasodilator
responses to various wines in all subjects (n = 53): EB vs. RST, WST, or alcohol:
ANOVA P < 0.001; EB vs. LB: ANOVA P = NS; LB vs. RST, WST, or alcohol: ANOVA
P < 0.001; RST vs. WST or alcohol: ANOVA P < 0.01; WST vs. alcohol: ANOVA
P = NS. (b) Vasodilator responses to various wines in normotensive subjects
(n = 27): EB vs. RST: ANOVA P < 0.01; EB vs. WST or alcohol: ANOVA P < 0.001;
EB vs. LB: ANOVA P = NS; LB vs. RST: ANOVA P < 0.05; LB vs. WST or alcohol:
ANOVA P < 0.001; RST vs. WST: ANOVA P = NS; RST vs. alcohol: ANOVA P = NS;
WST vs. alcohol: ANOVA P = NS. (c) Vasodilator responses to various wines
in hypertensive patients (n = 26): EB vs. RST: ANOVA P < 0.05; EB vs. WST or
alcohol: ANOVA P < 0.001; EB vs. LB: ANOVA P = NS; LB vs. RST: ANOVA P < 0.05;
LB vs. WST or alcohol: ANOVA P < 0.001; RST vs. WST: ANOVA P < 0.01; RST vs.
alcohol: ANOVA P < 0.01; WST vs. alcohol: ANOVA P = NS. ANOVA, analysis
of variance; EB, red wine produced “en barrique”; LB, red wine produced in
large wood barrels; RST, red wine produced in steel tanks; WST, white wine
produced in steel tank. Data are mean ± s.e.m.
steel tank or with alcohol alone. The vasodilation observed with
EB and LB does not seem to involve NO production because no
effect was observed after preincubation with an inhibitor of NO
synthase. A possibly relevant role might have been exerted by
components such as quercetin and tannic acid within the red
wines.5,6,9 For the production of the Albarello Rosso del Salento
(RST), the grapes are typically pressed and fermented without
grape stems, and the wine matures in steel tanks. The Barolo
Scarzello is matured in large barrels (LB), whereas the Barolo
Oberto is matured in small oak barrels (“en barrique”) (EB),
both of them for period longer than 1 year. We observed a significant vasodilatory effect of Albarello Rosso del Salento, but
this effect was less pronounced than the effect of the red wines
produced in wooden barrels. Therefore, prolonged contact
of the wines with the wood of the barrels enriches them with
376
50 µl
50 µl + L-NMMA
EB in all subjects
−53.0 ± 25.7***,†††,‡‡‡
−51.8 ± 28.1***,†††,‡‡‡
LB in all subjects
−48.5 ± 24.3***,†††,‡‡‡
−41.0 ± 25.6***,†††,‡‡‡
RST in all subjects
−33.1 ± 20.1***,†††
−29.1 ± 19.6***,†††
WST in all subjects
−18.0 ± 8.67‡‡‡
−16.2 ± 10.2‡‡‡
Alcohol alone in all
subjects
−15.5 ± 16.8‡‡‡
−16.5 ± 16.1‡‡‡
EB in NT
−55.6 ± 21.5***,†††,‡‡
−50.1 ± 28.4***,†††,‡‡
LB in NT
−43.4 ± 12.4***,†††,‡
−39.8 ± 18.4***,†††,‡
RST in NT
−28.1 ± 20.6†
−23.1 ± 19.2†
WST in NT
−15.5 ± 9.76‡
−12.4 ± 8.47‡
Alcohol alone in NT
−19.9 ± 7.68
−17.4 ± 12.7
EB in EH
−53.6 ± 28.8***,†††,‡
−55.2 ± 29.3***,†††,‡
LB in EH
−54.5 ± 26.5***,†††,‡
−45.6 ± 25.7***,†††,‡
RST in EH
−39.1 ± 19.9**,††
−34.9 ± 19.8**,††
WST in EH
−22.1 ± 5.43‡‡
−22.0 ± 10.6‡‡
Alcohol alone in EH
−12.0 ± 23.3‡‡
−16.8 ± 20.0‡‡
EB, red wine produced “en barrique”; EH, hypertensive patients; LB, red wine produced
in large wood barrels; NT, normotensive subjects; RST, red wine produced in steel tanks;
WST, white wine produced in steel tank.
**P < 0.01, ***P < 0.001 vs. alcohol alone; †P < 0.05, ††P < 0.01, †††P < 0.001 vs. WST;
‡P < 0.05, ‡‡P < 0.01, ‡‡‡P < 0.001 vs. RST.
substance potentially responsible for their marked vasodilatory
effects. In our study, Breganze Bianco, a white wine produced
in steel tanks (WST) had also a vasodilatory effect, but this
effect was much less pronounced than the vasodilatory effects
of red wines, and almost negligible. The observed vasodilatory
effect of red wines produced in wooden barrels (a technique
widely used in Italy and France) might reflect a more extensive
endothelium-protective properties, which could explain why
the effect of wine consumption on the mortality of myocardial
infarction is more pronounced in France and Italy than in any
other country,29,30 although this connection might be considered speculative. It is, however, interesting to hypothesize that it
might not only be the higher amount of wine that is consumed
in these populations but also the preferred choice of wine that
accounts for these differences. If conclusions are drawn from
epidemiological studies on the effects of wine consumption, the
important aspect of different effects of different wines has to be
taken into account, and it may also contribute to explain controversial findings in this regard.2,3,13
In the present study, we were unable to precisely characterize substances potentially responsible of the vasodilator effect
observed and provided by the contact with wooden barrels,
although quercetin and tannic acid are obvious candidates.14
Tannic acid and, to a minor degree, quercetin seem to exert
similar vasodilator effects on rat aorta and human coronary
artery.14 In the study by Flesch et al.,14 tannic acid caused an
endothelium-dependent vasodilation in rat aortic and human
coronary artery rings, of similar extent to that observed with
barrique-produced red wine, which was accompanied by
april 2010 | VOLUME 23 NUMBER 4 | AMERICAN JOURNAL OF HYPERTENSION
Vascular Function and Red Wines
an increase in vascular cGMP content and which could be
­abolished by L-NMMA. Thus, the effects of tannic acid on
human and rat arteries seem to be similar to the effects of
those wines that are known to have an especially high content
of tannins.14 Therefore, in our view, the most likely candidate
in explaining the observed vasodilator effects is tannic acid,
although other compounds may play a relevant role.
The vasodilatory effect of quercetin seems to be more complex to explain. Exposure to quercetin also leads to an increase
in vascular cGMP content, which can be attenuated by inhibition of the NO synthase.14 However, this does not seem to
be the relevant mechanism explaining its vasodilatory effect
because this vasodilatory effect was independent from the
integrity of the endothelium and could not be reversed by
L-NMMA,14 although some study suggested a partial dependency of the observed vasodilator response in the presence of
an intact endothelium.27
Whether the observed effects could be of relevance in vivo is
still partially a matter of debate. Tannins or phenolic substances
are absorbed from the intestine. Singleton et al.31 observed an
increase in serum tannic acid levels after addition of tannic acid
to animal food. Nigdikar et al. observed a marked increase of
polyphenolic substances in humans after intake of 275 ml of red
wine daily for 2 weeks.32 This amount corresponds to a plasma
concentration of polyphenols around 450 µg/ml that, in in vitro
study by Leikert et al.,5 was associated with a relevant biological activity. More recently, Spaak et al.33 could observe marked
plasma increases of resveratrol and catechin after intake of one
or two glasses of red wine. Brachial artery diameter increased
after both one and two alcoholic drinks (wine or alcohol alone).
No beverage augmented, and the second wine dose attenuated,
flow-mediated vasodilation.33
In our study, we investigated also patients with EH, considered as subjects at relatively high risk of cardiovascular
events, also in relation to the high prevalence of endothelial dysfunction in their small resistance arteries.20–22,34 In
effect, our essential hypertensive patients clearly showed the
presence of endothelial dysfunction, as demonstrated by the
observation of a reduced acetylcholine-induced vasodilation.
Therefore, this group should theoretically particularly benefit
the vasodilatory and vasculoprotective effects of red wines.
However, it was previously demonstrated that the effect of
red wine intake in blood pressure levels is complex. Only a
modest intake of alcoholic beverages seems to be beneficial
or neutral in this regard, and a linear relationship between
alcohol intake and blood pressure was observed in different populations, including regular alcohol drinkers, or NT
and hypertensive subjects.16,35 Intervention studies have
­consistently shown a reversible blood pressure–raising effect
of alcohol.16
Finally, our study demonstrated a significant ­vasodilation
induced by red wines in small resistance arteries of both NT
subjects and hypertensive patients, but failed to prove its
dependency on vascular NO production, because it was not
inhibited by L-NMMA. This is, at least in part, a difference
to what was previously observed in other studies, in which
AMERICAN JOURNAL OF HYPERTENSION | VOLUME 23 NUMBER 4 | april 2010
original contributions
wine polyphenols were demonstrated to be able to induce
­vasodilation by increased NO bioactivity.5,6,9 Also in the study
by Flesch et al.,14 the vasodilatory effects of red wines were
abolished after endothelial denudation and reversible by NO
synthase inhibition. However, as previously mentioned, when
effects of red wine intake on flow-mediated dilatation of the
brachial artery were investigated by a meta-analytic approach,
results were inconsistent.14 Therefore, this issue remains controversial. Possible explanations for the different findings may
be peculiar characteristics of subcutaneous small resistance
arteries, in respect to coronary arteries investigated by Flesch
et al.,14 or the possibility that vascular responses observed
in our study might have been endothelium-dependent, but
not NO dependent. In this regard, a possible candidate is
­endothelium-derived hyperpolarizing factor, which was demonstrated to mediate mediated relaxations induced by red wine
polyphenols in porcine coronary arteries.36
Finally, it is improbable, although it may not be completely
excluded, that, in our study, beneficial effects of red wines on
the vasculature might have been ascribed just to unspecific
vasodilator properties of alcohol content of different wines. It
should, however, be acknowledged that, in general, available
data show a remarkable risk reduction associated with moderate alcohol intake per se, although wine intake seems to have
some advantage compared with alcohol alone.1–3
In conclusion, our results suggest red wines are more potent
vasodilator than ethanol alone, possibly depending on the content of polyphenols or tannic acid. Hypertensive patients show
similar responses compared with NT controls, indicating that
red wine is not harmful in this population.
Acknowledgments: This study was partly financed by the European
Community’s Sixth Framework program “InGenious HyperCare.”
Disclosure: The authors declared no conflict of interest.
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april 2010 | VOLUME 23 NUMBER 4 | AMERICAN JOURNAL OF HYPERTENSION