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.1 ,n J C/in Nuir 1993:57 :213-7. Printed in USA . 1993 American Society for Clinical Nutrition 21 3
P lasm a ascorb ic ac id concentra tions re la te inverse lyto b lood pressure in hum an subjec ts13
John P Moran , Leslie (ohen, Jane M G reene, G uifa Xi,, E laine B Feldman,
Curtis G Ifames, and Dan iel S Feldman
ABSTRACT This study rela tes an tiox idant sta tus and blood
pressure (BP) in 168 healthy residen ts ofAugusta , GA, following
usual diets. BP ranges were systolic (5) 84-1 52 , m ean 1 12 1
mm Hg, and diastolic (D ) 52-96 , m ean 72 1 m m Hg. Plasma
concentrations ofascorbic acid (AA) were significantly inversely
rela ted to SBP (r = -0.18, P < 0 .05) and DBF (r -0.20, P
< 0 .0 1): w ith regression equations SBP vs AA= -0.083C
+ 1 16 and DBP -0.077C + 76. Highest and lowest quintiles
of AA differed significantly in mean SBP (108 2, 1 1 3 2 mm
Hg) and DBP (69 I, 74 2), P < 0 .05 . Plasma AA concen-
tra tions were significan tly lower in the smokers. By deleting
sm okers, the inverse rela tions ofSBP and DBF w ith plasma AA
and the slopes ofthe equation were enhanced. Plasma selen ium ,
ct-tocopherol. cs-tocopherol:cholesterol ra tio, re tinol and taurine
were not related to BP: whereas male gender, body mass index,
body fat distribution, plasma cholesterol, low density lipoprotein
cholesterol, and triglycerides correla ted. Am J C /in Nutr
1993:57:213-7.
KEY WORDS Ascorbic acid, blood pressure , antioxidants,
se lenium , taurine, a-tocopherol, re tinol, WBC ascorbic acid, vi-
tam in C, smokers
Introduction
The development of hypertension can be influenced by ge-
netic , hormonal, and nutritional factors( 1 ). Many studies haverela ted hypertension to intakes of sodium (2), po tassium (3),
calc ium (4), a lcohol (5), and energy (6). The role ofdietary an-
tioxidants in rela tion to b lood pressure (BP) is ofrecen t interest.
Epidem io logic data support an inverse association between cir-
culating antioxidants and blood pressure (7, 8). Salonen et al
(9) in a study of normotensive Finn ish men reported that BP
was moderate ly inversely associated with concen trations of
plasma ascorbic acid and serum selenium . There was marked
elevation of BP at the lowest concen trations of these nutr ients
(9). Other investigators in the United States and Japan have
reported that vitam in C nutriture was significantly inversely
correla ted with both diastolic b lood pressure (DBP) and systolic
BF (SBF ) (10 -12). McCarron et al (8) found that sign if icant
decreases in the consumption of vitam ins A and C were some
nutritional factors that distinguished hypertensive from nor-
motensive subjects. Studies in humans and rats have reported
that the am ino acid taurine decreases BF (1 3-1 5).
The purpose of this study was to test the hypothesis, on th
basis of the litera ture , that the BP of Georgians was inversely
related to the plasma values of the antioxidants ascorbic acid
selenium and cs-tocopherol and to exam ine the possib le asso
ciation between plasma retinol and taurine concentrations
w ith BP.
Subjects and m ethodsOne hundred sixty-eight healthy normotensive or asymptom -
atic hypertensive volun teer subjects were recruited from t
Augusta , GA, region. There were 108 women and 60 men: 1
were white and 16 were black. Their ages ranged from 19 to
y (1 SEM : 37 1). They were not taking an tihypertensive
medication and did not have heart disease , diabetes mellitus,
hepatic or renal disease, o r known hyperlipidem ia. They wer
consum ing their regular diets and ind icated that they were n
using supplements w ith ascorbic acid beyond the recommended
dietary allowances (I 6). Fifty-six subjects reported taking su
plements that included ascorbic acid . One subject was discovered
to be ingesting 3 g ascorbic acid /d after a high plasma concen-
tra tion (143 zmol/L) was assayed in the study. Further inqu iry
indicated that two subjects took supplements containing 1
ascorbic acid and three subjects took supplem ents of 500 , 25
and 200 mg, respectively. Inform ed consen t was obtained from
all subjects and the procedures followed were approved by an
are in accord w ith the ethical standards ofthe Human Assurance
Comm ittee at the M edical College ofGeorgia . Each subject fill
ou t a self-adm in istered questionnaire to provide data concerning
caffeine intake, a lcohol use, tobacco use, exercise , fam ily histor
ofhypertension, use oforal contraceptives or steroid hormones,
vitam in and/or m ineral supplement use, and demographics.
Standardized anthropometric m easurements ( 1 7) of body
heigh t and weigh t were obtained to enable calculation of th
body mass index (BM I, in kg /m2). Heigh t was m easured whil
I From the Departm ent of M edicine. Section of Nutrition. M edic
College ofGeorgia . Augusta, GA .2 Supported by NHLBI MERIT award (CGH) and summer researc
fellowship M CG (LC).3 Address reprin t requests to EB Feldman. Medical College of Georg
Departm ent of M edicine. Section of Nutrition, BG-230 , Augusta ,
309 12-3 102.
Received January 21. 1992 .
Accepted for publication August 10, 1992 .
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TAB LE 1
S tu dy v ari ab le s0
V alue
37.2 0 .8 6 (1 9-7 0)
1 . 7 0 . 0 1 ( 1 . 5 - 1 . 9 5 )
68.6 1 . 05 (4 3. 2 -1 0 7 .5 )
23.5 0 .3 ( 16 .4 -3 3. 2)
78.0 0 .8 5 ( 59 .5 -1 08 )
96.5 0.7 (76.2-14 1.6)
0.81 0 .0 05 ( 0. 66 -0 .9 7)
1 1 1 .6 0 .9 ( 84 -1 52 )
72.3 0 .7 (5 2-9 6)
5 0 . 5 1 . 7 ( 5 . 7 - 14 3 . 1 )
17.9 1 .5 9 ( 0. 37 -3 3. 1)
1 .42 0 .0 2 ( 0. 39 -2 .3 8 )I .7 0 .0 4 ( 0. 9- 2. 6)
23.7 0 .7 ( 11 .7 -5 4. 1)
60.8 2 .3 ( 26 .3 -1 4 7. 2)
4 . 8 0 . 0 1 ( 2 . 8 - 7. 3 )
1. 4 0 .0 3 ( 0.8 -2 .4 )
3. 0 0 .1 ( 1. 0- 5. 4)
1. 1 0 .0 6 ( 0.3 -2 .7 )
21 4 M ORAN ET AL
subjects s tood erect against the upright bar of the heigh t scale
and w ore no shoes. W eight w as m easured in the m orning befo re
eating w ith the subject dressed in ligh t clo th ing and w ithou t
shoes. T he sam e balance-beam scale w as used on all subjects.
W aist and hip girth w ere m easured w ith a tape m easu re and the
w aist-to -hip g irth ratio w as calculated .
BF w as assessed in the m orning af ter 5 mm rest and before
other m an ipulations. T hree m easu rem en ts w ere tak en w h ile
sub jects w ere in the seated position by using a T ay lo r au tom ated
digital read ou t sphy gm om anom eter (S y bron Corpo ration ,
R ochester, N Y ). A n av erage o f the three B F read ings w as cal-
culated.
B lood sam p les w ere obtained from each subject in the m orning
af ter a 1 2 - 14-h ov ern ight fast by using ev acuated tubes con -
tam ing sod ium heparin (143 USP units/tube) or EDTA as an-
ticoagu lant. T he b lood w as prom p tly centrifuged fo r 1 5 mm at
800-850 Xg at 4 #{ 176} Co separate the p lasm a. Hepariniz ed p lasm a
sam ples w ere stored at -25 #{ 176} C ,rotected f rom light ex posure,
f or 2 m o. T his plasm a w as assay ed for ascorb ic acid , selenium ,
a-tocopherol, retinol, and tau rine. EDTA plasm a w as assay ed
for to tal cho lesterol and trig ly cerides . H igh-density -lipopro tein
(HDL ) cholesterol w as quantitated af ter p recipitation by using
dex tran m agnesium sulfate. L ow -density -lipopro tein (LDL )
cholesterol w as calculated by using the form u la
LDL cholesterol = t ot al c ho le st ero l - HDL cholesterol
- (trig ly cerides X 0.16).
T he p lasm a ascorb ic acid concentration w as quan tif ied by
using a co lo rim etric phosphotungstic acid assay in operation in
the N utrition L aboratory (1 8). T he plasm a selenium concentra-
tions w ere determ ined by using a f luorom etric m ethod of W hetter
and U llrey (19). In a random subset o f 82 subjects , the plasm a
a-tocopherol and retinol concen trations w ere determ ined si-
m ultaneously by the HPLC m ethod ofCatignani and B ieri (20).
In a random subset of 108 subjects , p lasm a tau rine concentra-
tions w ere determ ined by the HPLC m ethod o f H ill et al (21).
C holesterol and trig ly cerides w ere determ ined w ith a co lo ri-
m etric-enzym atic m ethod on the O lym pus D em and C lin ical
C hem istry A naly z er (O lym pus Corporation, N ew Y ork , N Y ).
T hree-day food-intak e reco rds (including d ietary supp lem ents)
w ere ob tained from 25 subjects w ith v alues in the low est and
highest quintiles ofplasm a asco rbic acid , p lasm a selenium , and
BF. A reg is tered dietitian instructed the sub jects on com pleting
the food d iaries , w hich w ere recorded on tw o w eek day s and one
w eek end day . The dietitian w as certif ied by the Un iv ersity o f
M innesota N utrition Coordinating C enter in the adm inis tration
and v alidation rev iew of the food records. T he data w ere analy z ed
and nutrient in tak es quantitated by the com puter program at
the M innesota C en ter. T he 3-d food reco rds w ere repeated andblood sam ples w ere obtained . Plasm a ascorbic acid concentra-
tions w ere repeated and w hite blood cell ascorbic acid concen-
trations w ere m easu red by using the colorim etric pheny lhy dra-
z inc m ethod of Denson and B ow ers (22).
T he data w ere analy z ed w ith the M acIntosh com pu ter statis-
tic al p ro gram s Stat View II an d Super ANOVA (A bacus C on-
cepts, B erk eley , CA ). T he low est and highest quintiles for the
nutrient concen trations w ere identif ied and SB P and DB P w ere
com pared for these subjects by using the S tudentst test. The
data w ere also ev aluated by regression analy sis, w ith the m ean
SB P or DB P as the dependent v ariable and w ith v alues of each
of the nutrients stud ied.
Results
The v ariab les ex am ined in the 168 subjects arc included i
T able 1. T he SB P ranged from 84 to 152 mm Hg (m ean 1 1
1 ). Plasm a ascorbic acid concentrations w ere 1 1% higher insupplem ent users than in nonusers.
SB P and DB P readings of m en w ere 8 and 6 mm Hg h igher,
respectiv ely , th an those ofw om en (P < 0.02). In obese subjects
(m en w ith a BM I> 27.8, w om en w ith B M I> 27.3) SB F w as 3
mm Hg higher (1 14.6 2.4 , 1 SEM ) than in nonobese subjects
(1 1 1 .4 0.97). DBP w as 7 mm Hg higher (79 2.1) in obese
than nonobese subjects (72 0 .7 ,P = 0.001).
Plasm a concentrations of ascorb ic acid w ere sign if icantly in
v ersely related to SB P(r = -0 . 1 8, P < 0.05) and DB F (r= -0 .20, P < 0 .01 ). T he regression equations indicated that fo r
a l00-m ol/L increase in the plasm a asco rbic acid v alue, bo th
SBF and DB P decreased by 8 mm Hg (Fig1) . S ubjects in the
highest and low est qu in tiles of plasm a ascorbic acid had signif
icantly dif ferent SB F (108 2 and 1 13 2 mm Hg,P < 0.05)
and DB F (69 1 and 74 2 mm Hg,P < 0.05; Fig 2) readings.
The plasm a m ean ascorbic acid concentration s w ere signif icantly
(30% ) low er (34 v s 5 1m o l/L ) in the 10 m oderate and 2 heav y
(> 20 cigarettes/d ) cigarette sm ok ers than in the nonsm ok ers.W e determ ined the relation of plasm a ascorbic acid and B P
sm ok ers and nonsm ok ers . In nonsm ok ers , com pared w ith th
to tal group, the inv erse correlation of asco rbic acid w ith SB F
A ge(y )(n = 168)
Height(m )(n= 168)
W eight (k g )(n = 168)
B ody m ass index t(n = 168)
W aist circum ference (cm )(n - 167)
Hip circum ference (cm )(n = 167)
W aist-to-hip ratio(n - 167)
S y stolic blood p ressure (m m Hg)
(n = 168)
D iasto lic blood p ressure (m m Hg)
(n = 1 6 8 )
A scorbic acid (M m ol/L )(n = 168)W hite blood cell ascorbic acid
(zg/l06 WBC ) (n = 22 )
S elenium (M m ol/L )(n = 168)R etino l (M m ol/L )(n = 82 )
a-T ocophero l (M m ol/L )(n = 82 )
T au rine (M m ol/L ) (n = 108)
T otal cho lesterol (m m ol/L )(n = 101)
HDL ch olesterol (m m ol/L ) (n = 101)
L DL cholesterol (m mol/L )(n = 101)
T rigly cerid es (m m ol/L ) (n = 101)
0 SEM (range). B iochem ical v alues are f rom p lasm a unless oth
erwise specified .
t In k g/m 2 .
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15 0
1 30
1 1 0
90
7 0
I
EE
LU
LU
a .000-j
I
EE
LU
U)Cl )LU
a.
000-j
0-j
0I-Cl )
U)
a )
I
EE
LU
Cl)U)LU
a.
000-J
0-J
0I.-U)4
0
Vita m in C ( m o Ie s /L)
PLA SMA ASCORBIC ACID AND BLOOD PRESSURE 215
FI G 1 . Relationship between plasma ascorbic acid and systol ic anddiastol ic blood pressure in men (#{ 149} )nd women (s). The solid l ines
represent the regression equations, w hich w ere signi f icant for systolic(P
= 0.02) and diastol ic blood pressures(P = 0.008).
w as increased to r = -0.25 (P = 0.002) and for DBF increased
to r = -0.27 (P = 0.0009). In the nonsmokers, the slope of theregression equation for SBP was greater than that for the total
study population, indicating a 12-mm Hg decl ine in SBP per
100 zmol /L ascorbic acid(P = 0.002). The slope ofthe regression
equation for DBP simi larly was greater w i th a 10-mm decline
in DBP per 100 Mmol /L ascorbic acid(P = 0.0009). In the smok-ers, the relation ofplasma ascorbic to SBP and DBP was reversed,
compared w i th nonsmokers, so that the correlations were posi tive
(r = 0.75, SB P: r = 0.67, DBP) and the slope of the regression
w as posi ti ve (P = 0.009, P = 0.004). When smokers were deleted
from the highest (3 smokers) and lowest (3 smokers) quinti l es
ofplasma ascorbic acid, the di fference in thei r BP was enhanced:
SBP 107 2 and 1 15 2 mm Hg(P - 0.001) and DBP 69
1 and 76 2 mm Hg(P < 0.01). The plasma ascorbic acid
concentrations were inversely related to body-fat di stribution
(w ai st-hi p rati o): r -0.3, P < 0.002.
S Y S TO LIC DIA S TOL IC
FIG 2. Individual measurements of systol ic (lef t) and diastolic (righblood pressure in subjects in the lowest (0) and highest (#{ 149} )uinti l es ofpl asm a ascorbi c aci d concentrati on. Shaded areas represent 1 SD aboutthe mean blood pressure (horizontal l ine). The low est quinti le of plasm
ascorbic acid w as 5.6-24.5 M mol /L : the highest quinti l e ofplasma ascorbacid was 85. 1-143 M mol/L . The mean blood pressures ofsubjects in tl ow est and highest qui nti les di ff er si gni fi cantl y(P < 0.05).
V ariables that w ere signi f icantly related to SBP and/or DBP,
respectively, (Table 2) included body-fat di stribution (waist-hip
girth, r = 0.37, 0.32: P < 0.001). BM I (r = 0.39, 0.40: P
< 0.001), plasma cholesterol (r = 0.28, 0.32; P < 0.01), LDL
cholesterol (r = 0.25, 0.3 1 ;P < 0.01 ), and t ri g ly cer i des (r = 0.20,
P< 0.05).
We also carried out mul tiple-l inear-regression analysi s. in
cluding data from al l subjects, of the association between SBF
and DBP wi th plasma ascorbic acid, BM I, and total cholesterol .
Parti al correlation coeff icients were signi f icant for SBP and DB
w ith BM I (P = 0.001, P = 0.0001) and total cholesterol (P
= 0.03, P = 0.01). When smokers were excluded, the value of
the coeff icient for ascorbic acid increased inversely to correlate
TABLE 2Correlation coeff icients of anthropometric measurements and blood
antioxidant and blood l ipid concentrations wi th blood pressure
Systolicb lo od p ressu re
Diastolicb lo od p ressu re
B ody mass index (n = 168) 0 .390 0.400Wai st-to-hip rati o(Fl = 167) 0.37 0.320
Plasma ascorbic acid(n = 168) -0.181 -0.20jW hi te blood cel l ascorbic acid
(I = 122) -0.26 -0.26
Retinol ( 1 = 82) 0.24t 0.22ta-Tocopherol (n = 82) 0.01 0.06Selenium (n = 168) 0.10 0.12
Taurine (F? = 108) 0 -0.03To tal cho l est erol (n = 101 ) 0.28t 0.324HDL chol est er ol (n = 101) 0.02 -0.07
LDL chol esterol (a= 10 1 ) 0.25j 0.3 1j
Triglycerides (n = 101) 0.16 0.20t
*P =
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21 6 M O R AN E T AL
signif icantly w ith SB P(P = 0.04) and w ith DB P (P = 0.03);cho lestero l no longer correlated sign if icantly w ith DB P. Further
ev idence that v itam in C am ong 1 2 v ariables in the data set in-
dependently negativ ely inf luences B P in nonsm ok ers w as ap-
paren t by factor analy sis (data not prov ided).
T here w as no sign if icant association betw een B P and plasm a
selenium , a-tocopherol, the ratio o fa-tocophero l to cholesterol,
p lasm a retinol, or tau rine concentration s. T he data f rom 3-d
food d iaries indicated the m ean daily d ietary in tak e of v itam inC ex clusiv e ofsupplem ents w as 86 10.6 m g and of selenium
w as I 22 1 1. I g . In tak e of these antiox idants (diet p lus sup-
plem ents) did not correlate signif icantly w ith plasm a concen-
trations nor w ith B P, possib ly because of the low er subject num -
ber. W hite blood cell asco rbic acid concentrations w ere directly
related to plasm a ascorbic acid concen trations (r = 0.43, P< 0.05), but did not correlate signif icantly w ith B P.
Dis cus s ion
This study indicates that plasm a asco rbic acid concentrations
in healthy G eorgians w ith SB P< 160 mm Hg and DB P< 10 0
mm Hg (no treatm en t) w ere inv ersely related to SB P and DB P.T he results agree w ith prev ious repo rts that hav e described a
sim ilar relationship . A recent rev iew of the w orld literature in-
cluded sev en studies f rom the United S tates, Finland, and Japan,
involving > 12 000 subjects (23 ). In all the popu lations, ascorbic
acid nutriture w as signif ican tly inv ersely correlated w ith both
SB P and DB P. T he largest s tudy included> 10 000 peop le and
relied on 24-h dietary recalls to estim ate the ascorbic acid in tak e
o f the sub jects. S uch data are im precise but data f rom 1 7 00
subjects hav e related B P to the fasting plasm a ascorb ic acid con-
centration as the indicator of ascorbic acid statu s. In m ost in-
s tances, in contrast to this study . the inv estigators d id not repo rt
the status of o ther nutrien ts that m ay relate to blood pressure.
S ev eral th eo ries hav e been proposed to ex p lain the association
o f plasm a ascorbic acid concentration s w ith B P. T he role of
ascorbic acid as an antiox idant and its ef fect on o ther nutrients
hav e been em phasiz ed. A s an antiox idant, ascorbic acid inf lu-
ences p rostaglandin production, w hich in tu rn af fects blood
pressu re. S om e prostaglandins, such as prostacy clin (PGI-2), are
v asodilato rs and are therefore hy potensiv e. O ther pro staglandins
arc v asoconstricto rs, lik e throm box ane A -2 (TX A -2) and are
hy pertensiv e. Prostagland in s are sy nthesiz ed from po ly unsatu -
rated fatty acids (PUFA s), especially linolcic acid , and PUFA s
are suscep tib le to autoox idation. O xy gen and hy drogen perox ide
can act on PUFA s and cause the form ation of f ree radicals and
m alondialdehy de, and perox idiz ed fats can retard the production
ofTX A -2. T hus, antiox idan ts that p rev ent the autoox idation of
lip ids m ay hav e an antihy pertensiv e ef fect. T here is som e cv i-
dence that antiox idants increase the production of PG I-2 (24).A ccording to Frei ct al(25), ascorbate is the m ost ef fectiv e
aqueous-phase antiox idant in hum an blood p lasm a. A scorbate
not only com pletely pro tects the lip ids f rom detectable perox i-
dativ e dam age but also spares a-tocopherol, w hich also has an-
tiox idant activ ity . A scorbic acid w ork s sy nergis tically w ith v i-
tam in E to p rev ent the autoox idation o f PUFA s in a radical
cascade (26). L ow concentrations of ascorb ic acid lead to de-
creased conv ersion o f v itam in E rad ical to v itam in E , w hich
m ay cause an increase in perox idiz ed fats .
S alonen et al (9) found that decreased plasm a ascorb ic acid
concentrations w ere associated w ith reduced plasm a concentra-
tions of 6 -k eto-prostaglandin-F-la, the m etabolite o f prostacy -
din . T h is observ ation supports the theory that dietary an tiox i-
dants enhance the production o fprostacy clin by scav enging f r
radicals and perox ides, w h ich inhibit prostacy clin sy nthetase
concentration s abov e a certain threshold .
T rou t (23 ) suggested that plasm a ascorbic acid m ay low er
b lood pressure in part by altering leuk otrienc m etabolism , be
cause earlier w o rk reported a positiv e association betw een seruma-glu tam y ltranspeptidase (a-GTP) and B P and a negativ e as
sociation betw een plasm a ascorbic acid and a-GTP( I 2 ).A scorbic acid m ay affect B P by inf luencing other nutrients,
such as sodium . K oh( 10) p roposed that ascorbic acid is ef fectiv ein hy pertensiv e patien ts by low ering sodium content in the blood
She also suggested that the hy potensiv e function ofascorbic ac
m ay result f rom decreasing norepinephrine release f rom nerv e
endings and from the adrenal m edulla in consequence o f low
ex changeable sodium content in the circulation.
T hus, serum asco rbic acid m ay sim ply ref lect the intak e o
other im portant nutrients that inf luence B P, such as potassium
and d ietary f iber. T hese nutrients increase w ith the f requent
consum ption o f f ruits and v egetables (1 2). T he low er intak e
ascorb ic acid in hy perten siv e subjects m ay ref lect in part thclose association of asco rbic acid and potassium intak e (8). Po
tassium consum p tion and its relation to sodium intak e are other
im portant nutrient inf luences on B P (3 ).
S ev eral sm all in terv ention studies using v itam in C hav e y ielded
v arious ef fects on B P. A scorbic acid supplem en tation ( 1000 m gd for 3 m o) reduced both SB P and DB P in 23 m ildly hy pertensiv e
w om en (10). A study cited by T rout (23) of I 2 m ildly hy perten-
siv e subjects supp lem ented w ith 1000 m g ascorbic acid/d for
w k only rev ealed a decrease in SB P. A sco rbic acid supplem en-
tation d id not change B P in a study o f healthy y oung w om en
cited by K oh (10).
I t has been suggested that hy pertension itself enhances the
m etabolism of ascorbic acid (1 2), such as the ef fect ascribed
sm ok ing and plasm a ascorb ic acid concentrations. T he presents tudy con f irm ed a signif icantly low er concentration of p lasm a
asco rbic acid concentration in sm ok ers as has been dem onstrated
in num erous studies . T his association persists despite correction
for factors that independen tly af fect serum ascorbic acid con-
centration s (age, sex , race, B M I, dietary ascorbic acid intak e,
and alcoho l consum p tion ). Conf licting m echanism s hav e bee
proposed to ex plain the ef fect ofsm ok ing. S om e stud ies rev ealed
increased m etabo lism ofasco rbic acid in sm ok ers, w ith increased
turnov er and increased urinary ex cretion . O ther studies found
im paired ascorb ic acid absorption bu t norm al turnov er(27).
In this study , p lasm a ascorbic acid concentrations w ere in
v ersely related to m easures and distribution of body fat (BM I
and w aist-h ip ratio). T hese index es f or obesity w ere signif icantly
correlated w ith B P. Plasm a asco rbic acid has been reported pre-v iously to hav e a negativ e relationsh ip w ith obesity (1 1 ). T hi
relation is as y et unex p lained.
C onf licting results hav e been reported concerning the asso-
ciation ofselenium w ith B P. In th is s tudy plasm a selenium con
centrations did not correlate w ith B P, obesity , o r sm ok ing. T hes
resu lts are sim ilar to those of a Du tch study (28) that show ed
no relation ofselcn ium to B P but reported low er plasm a selenium
concentrations in sm ok ers . O ther studies reported that serum
selenium concentrations w ere m oderately inv ersely associated
w ith B P in hum ans (9 ). D ata f rom our labo rato ry rev ealed that
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PLA SM A A SCORB IC A C ID A ND BLOOD PR ESSUR E 21 7
the m ean B P of selenium -dep leted hy pertensiv e rats w as signif -
ican tly higher than the B P ofselenium -supplem entcd rats (29).
In contrast to other studies that reported an inv erse association
of B P w ith the am ino acid taurine, and a reduction in B P w ith
taurine supplem en tation (1 3, 1 5, 30, 3 1), no association w ith
taurine and B P w as found in this s tudy .
SB P and DB P m easured in 168 healthy A ugustan s consum ing
their usual diets w ere sign if icantly inv ersely related to their
plasm a concentrations ofasco rbic acid . T he m ean B P in subjectsin the low est quintile of plasm a ascorbic acid w as signif icantly
(5 mm ) higher than B P in subjects in the h ighest quintile of
v itam in C . Plasm a asco rbic acid concentrations w ere signif ican tly
reduced by 30% in sm ok ers. Plasm a ascorbic acid v alues w ere
inv ersely related to m easures and distribution ofbody fat (B M I
and w aist-h ip ratio). T hese index es ofobesity w ere signif icantly
correlated w ith B P. Plasm a selenium , a-tocophero l, th e ratio of
a-tocophero l to cholesterol, retinol, and taurine show ed no sig-
nif icant relationship to B P. In a subset of 25 subjects, th eir 3-d
reported dietary intak e did not correlate w ith blood concen tra-
tions o f antiox idants nor w ith B P.
T hese m easurem ents prov ide a basis to ex pand the study pop-
ulation to include m ore black s and o lder peop le at h igher risk
of hy pertension. Interv ention studies should be designed andundertak en to ev aluate the ef fects on B P of ascorbic acid sup-
plem entation in healthy subjects. If suggestiv e, these should be
ex tended to a double-blind, random ized con tro lled study o f pa-
tients w ith m ild to m oderate uncom plicated hy pertension as
part of a nonpharm acologic interv ention trial (32 ). B
Re f e r e n c e s
1. Feldm an EB . Essentials o fclin ical nutrition . Philadelphia: FA Dav is
C om pany , 1 988:45 5-7.
2 . E llio tt P. O bserv ational studies of salt and blood pressure. Hyper-
ten sion 199 l:17 (S uppl 1):I-3-8 .
3. C appuccio FP, M acG regor GA . Does po tassium supplem en tation
low er b lood p ressure? A m eta-analy sis ofpublished trials. I Hy pertens
1991:9:465-73.4. M ik am i H , Ogihara T , T abuchi Y . B lood pressu re response to dietary
calcium interv ention in hum ans. A m I Hyperten s 1990:3:1475-5 1 5 .
5 . K eil U . Cham bless L , Filip iak B , H artel U . A lcohol and blood pres-
sure and its in teraction w ith sm ok ing and other behav ioral v ariables:
results f rom the M ON ICA A ugsbury Su rv ey 1984-1985. 1 Hy pertens1 99 1 : 9: 4 9 1 - 8.
6. S cho tte DE , S tunk ard A l. T he effects ofw eight reduction on blood
pressure in 301 obese patients . A rch Intern M ed 1990:150 :1701-4 .
7 . S tanton IL , B raitm an LE , R iley A M , K hoo C -S , Sm ith IL . D c-
m ograph ic, d ietary , lif e sty le, and anthropom etric co rrelates of b lood
pressure. H ypertension 1982;4(suppl 3):l35-42.
8. M cCarron DA , M orris CD , H enry H I, S tanton IL . B lood pressure
and nutrien t in tak e in the United S tates. S cience 1984;224: 1392-8.
9 . S alonen IT , S alonen R , Ihanainen M , et al. B lood pressu re, d ietary
fats , and antiox idants . A m I C lin N utr 1988:48:1226-32.
10. K oh ET . Ef fect of v itam in C on blood param eters of hy perten siv e
sub jects. I Ok la S tate M ed A ssoc 1984;77: 177 -82.
1 1. K oh ET , Chi M S . R elationsh ip of serum v itam in C and globu lin
f raction s w ith anthropom etric m easurem ents in adults . N u tr R ep
In t 1 9 8 0: 21 :5 3 7 -4 9 .
12. Y oshiok a M , M atsushita T , Chum an Y . Inv erse association ofserum
ascorb ic acid lev el and blood pressure o r rate of hy pertension
m ale adults aged 30-39 y ears. In t I V itam N utr R es 1984:54:343 -
7.
13 . Fujita T , A ndo K , N oda H , Ito Y , S ato Y . E ffects o f increased a
renom edullary activ ity and taurine in y oung patien ts w ith bo rderline
hy pertensio n. C irculation 1987 ;7 5:525-32.
14 . Ogaw a M , T ak ahara A , Ishijim a M , T az ak i S . Decrease of plasm
su lf ur am ino acids in essential hy perten sion. Ipn C irc I 1985:49
1 2 1 7- 24 .
1 5. Inque A , T ak ahashi H , L ee L , et al. R etardation of the dev elopm ent
ofhy pertension in DO CA salt rats by taurine supp lem ent. C ardiov as
R es 1988 ;22:35 1-8 .
16. N ational R esearch Council. R ecom mended dietary allow ances. 1
ed. W ashington , DC : N ational A cadem y Press, 1989.
17. Feldm an EB . Essentials o fclin ical nutrition . Ph iladelphia: FA Da
C o. 1 98 8:6 4- 8.
18 . K y aw A . A sim ple colorim etric m ethod for ascorb ic acid determ i
nation in blood p lasm a. C lin Chim A cta 1978:86 :153-7.
19. W hetter PA , U lIrey , DE . Im prov ed f luorom etric m ethod for det
m in ing selenium . I A ssoc O f fA nal Chem . 1978;61 :927-30 .
20. C atignani GL . B ieri 1G . S im ultaneous determ ination o fretinol a
a-tocophero l in serum or plasm a by liqu id chrom atography . C li
C hem 1 98 3:2 9:7 08 -1 2.21. Hill DW , W alters FH , W ilson TD , S tuart ID . H igh perform ance
liqu id chrom atographic determ ination o f am ino acids in the pico
m ole range. A nal Chem 1979 :51:1338 -41.
22. Denson KW , B ow ers EF. T he determ ination of ascorbic acid
w hite b lood cells . A com parison ofW BC ascorbic acid and phenoli
acid ex cretion in elderly patien ts . C lin S d 1961:21:157 -62.
23. T rout DL . V itam in C and cardiov ascular risk factors. A m I C lNu t r 1 99 1: 5 3 : 3 22 5- 5 5 .
24. Sm ith R S. N utrition , hy pertension and cardiov ascular disease. G
roy , CA : T he Lyncean Press, 1984:2-7 .
25. Frei B , England L , A mes B . A scorbate is an outstanding antiox idan
in hum an blood plasm a. Proc N atl A cad Sci USA 1989 :86:6377 -
81 .
26. G ey K F, S tahelin HB , Pusk a P. Ev ans A . R elation ship of plasm
lev el ofv itam in C to m ortality f rom ischem ic heart d isease. A nnaof the N ew Y ork A cadem y of S ciences, 1987:498: 1 10 -23.
27. S chectm an G , B y rd IC , G ruchow HW . The in f luence of sm ok in
on v itam in C status in adults. A m I Public H ealth 1989 :79:158-62.
28. B uk k ens A U , deV os N , K ok Fl, S chouten EG , deB ruijn A M , H
m an A . S elenium status and cardiov ascular risk factors in healthy
Du tch subjects . I A m Coll N utr 1990:9:128-35.
29 . Feldm an EB , Carro ll R M , M artin W D, R ussell B S , Ham es C
Selenium status and blood pressure in the spontaneously hy pertensiv e
rat. In : Com bs GF Jr. S pallholz JE , L ev ander OA . O ldf ield JE , ed
Selenium in b io logy and m edicine. Part A . N ew Y ork : A VI, 1983 8 1 - 92 .
30. A be M , Y am ada TK . Fu ruk aw a T . -y -am inobuty ric acid and tau rin
antagoniz e the cen tral ef fects of ang io tensin II and renin on th
in tak e ofw ater and salt, and on blood p ressure in rats . N europhar-
m a co lo gy 1 98 8:2 7:3 09 -1 8.
31 . Fujita T , S ato Y . H ypo tensiv e ef fects o f tau rine. Possible inv olv em en
of the sym pathetic nerv ous sy stem and endogenous op iates. I C
I nv e st 1 9 88 ;8 2:9 9 3- 7.
32. B ulpitt C I. V itam in C and b lood pressu re. I H ypertens 1990 ;
1071-5.