am j clin nutr 1993 moran 213 7

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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.

am j clin nutr 1993 moran 213 7

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