Sodium Excretion and Racial Differences in Ambulatory Blood

813
Sodium Excretion and Racial Differences in
Ambulatory Blood Pressure Patterns
Gregory A. Harshfield, Bruce S. Alpert, Derrick A. Pulliam, Elaine S. Willey,
Grant W. Somes, and F. Bruder Stapleton
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The influence of Na+ excretion and race on casual blood pressure and ambulatory blood
pressure patterns was examined in a biracial sample of healthy, normotensive children and
adolescents (10-18 years; n=140). The slopes relating 24-hour urinary Na + excretion to systolic
blood pressure were different for both black and white subjects for casual blood pressure
(/><0.001) and blood pressure during sleep (/?<0.03). For casual blood pressure, the slope was
significant for black subjects (/3=0.17;/»<0.001) but not for white subjects. For blood pressure
during sleep, the slope was again significant for black subjects (/3=0.08; p<0.0l) but not for
white subjects. Na+ excretion was also related to awake levels of systolic blood pressure for
black subjects (/3=0.08, r=0.36;/?<0.01), although the slopes for both black and white subjects
were not significantly different. Further analyses indicated the results were not due to racial
differences in 24-hour urinary K+ excretion. However, plasma renin activity was marginally
related to Na + excretion in white subjects (r=0.22; p<0.06) but not black subjects, a finding
that is consistent with previous studies. Na + excretion was not associated with diastolic blood
pressure or heart rate in either group under any condition. The results of this study support
research that has demonstrated a stronger relation between Na + handling and casual blood
pressure in black subjects and extend these findings to blood pressure while the subject is both
awake and asleep. (Hypertension 1991;18:813-818)
ecent studies in both adolescents1 and adults2'3
demonstrated that black subjects as a group
had a "blunted" nocturnal decline in blood
pressure (BP). Research has shown that Na + intake is
a primary determinant of BP in a significant percentage
of both the hypertensive45 and normotensive 67 populations, a characteristic referred to as "salt sensitivity."
Furthermore, the prevalence of salt sensitivity has been
found to be greater in the black population than in the
white population.4-8 Therefore, the purpose of the
present study was to examine the effect of sodium
excretion (UNaV) and race on casual BP and ambulatory BP patterns in healthy black and white adolescents. In addition, K+ excretion (U K V) 9 - U and plasma
renin activity (PRA) 12 - 16 were measured to determine
the role of these factors that are known to influence
Na + homeostasis and BP control.
R
From the Department of Pediatrics (G.A.H., B.S.A., D.A.P.,
F.B.S.), and the Department of Biostatistics and Epidemiology
(E.S.W., G.W.S.), University of Tennessee, Memphis, Memphis,
Tenn., and the Department of Pediatrics (F.B.S.), SUNY at
Buffalo, Buffalo, N.Y.
Supported by grants HL-35788, HL-42645, and GCRC M01RR0021 from the National Institutes of Health.
Address for correspondence: Gregory A. Harshfield, PhD, University of Tennessee, Memphis, 848 Adams Ave., Memphis, TN 38103.
Received January 26, 1990; accepted in revised form July 23,
1991.
Methods
Subject Characteristics and Casual Measurements
The protocol was approved by the Institutional Committee on Human Research and the Clinical Research
Center Scientific Advisory Board. Written, informed
parental consent was obtained before testing. The
subjects were 199 healthy, normotensive children and
adolescents recruited from churches, schools, and social organizations as described in detail.17 Of these, 19
subjects (10%) were excluded from the analyses due to
questionable 24-hour recordings (see below); 40 subjects (20%) were excluded due to inadequate 24-hour
urine collections (see below). Excluded subjects were
similar in age, gender, BP, heart rate (HR), body
surface area (BSA), and PRA to subjects included in
the analyses. Health status was evaluated based on the
subject's medical history and a brief physical examination to rule out the presence of cardiovascular or other
abnormalities. The demographic characteristics and
casual measurements from the subjects included in the
analyses are provided in Table 1.
Casual Blood Pressure and Heart Rate
Casual BP and HR measurements were obtained
with the Dinamap BP monitor (model 1846SX, Critikon, Tampa, Fla.) before the ambulatory BP re-
814
TABLE 1.
Hypertension Vol 18, No 6 December 1991
Demographic Characteristics and Casual
Measurements
Variable
Sample size
Age (yr)*
Gender (male/female)*
Body surface area (m2)t
Sodium excretion (meq/24 hr)
Potassium excretion (meq/24 hr)t
Plasma renin activity (ng/ml/hr)
Black
White
66
74
14.0±2.4
30/36
1.61±0.26
144.4±48
34.8±2
3.4±2.4
12.6±2.2
45/29
1.51+0.29
129.4 ±54
42.6±2
3.2±2.0
Values are mean+SD.
*Black subjects differ from white subjects; /><0.05.
tBlack subjects differ from white subjects; p<0.01.
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cording procedure. The casual measurements were
the average of three readings taken in the seated
position after 5 minutes of sitting quietly.
Ambulatory Blood Pressure Recordings
The ambulatory BP recording procedures used in
our laboratory have been described in detail.1 In brief,
the subject was seated, and the ambulatory BP recorder (model 5200, Spacelabs Inc, Redlands, Wash.)
was applied and calibrated. The functioning of the
recorder was demonstrated to the subject, and the
details of the protocol described. The subject was
instructed to relax his or her arm during a BP determination and to provide diary information for each
hour the monitor was worn. The subject was then
instructed to resume his or her normal daily activities
and to return the following day for the removal of the
recorder. The recorder was set to take a reading at
20-minute intervals between the hours of 6:00 AM and
midnight and 60-minute intervals between the hours
of midnight and 6:00 AM. A successful recording was
one in which less than 25% of the readings during the
recording were considered artifacts,1 and the subject's
recording had data for at least 20 hours of the day.
Hourly averages were computed for each individual
and coded according to whether the subject was awake
or asleep during the hour. The average level of BP
while awake and asleep was then determined for each
individual based on the hourly averages.
Twenty-Four—Hour Urine Collection
The procedures for urine collections and analyses
have been described in detail.18 In brief, urine containers with boric acid preservative were provided for
the 24-hour urine specimens. Instructions (written
and verbal) on proper 24-hour urine collection were
given to each subject and parent before the procedure. Subjects who had 24-hour urine volume greater
than 500 ml and creatinine clearance greater than 75
ml/min/1.73 m2 were considered to have an adequate
urine collection and were included in the analyses.
Plasma Renin Activity
The procedures for the collection and measurement
of PRA and creatinine in our laboratory have been
described in detail.18 In brief, the subjects were seated
for 30 minutes before blood collection; while the subject was in the seated position, plasma samples were
drawn at 7:00 AM in tubes containing EDTA, which
were then immediately placed on ice. The samples
were centrifuged at 4°C and stored at -60°C until
analyzed. PRA was measured in duplicate by methods
described by Haber et al19 using radioimmunoassay kits
(Baxter Healthcare Corp., Cambridge, Mass.).
Data Analyses
Comparisons of subject characteristics were performed by analysis of variance on a Macintosh SE/30
computer with SUPERANOVA (Abacus Concepts Inc.,
Berkeley, Calif.). Overall analyses were performed by
analysis of covariance using the SUPERANOVA program, using Type III sums of squares to test for main
effects and interactions. The general form of the
models included three factors: 1) race, 2) UNaV as a
continuous variable, and 3) the interaction between
race and UNaV to test if the slopes relating UNaV to
BP in both black and white subjects were similar.
(Note: when one of the independent variables is
continuous and the other binary, the interaction term
represents a test of the equality of the slopes between
the two groups.) BSA was also included as a covariate in the models. The dependent variables included:
1) casual systolic BP (SBP), diastolic BP (DBP), and
HR; 2) SBP, DBP, and HR while the subjects were
awake; and 3) SBP, DBP, and HR while the subjects
were asleep. Planned comparisons examining the
slopes between UNaV and each dependent variable
for both races were performed. A value of p<Q.0l
was considered significant. In addition, analyses were
performed to test the relation between UNaV and
both UKV and PRA. Finally, separate models were
run substituting UKV for UNaV in the general model
to examine the relation between UKV and ambulatory BP patterns.
Results
Race, Age, Gender, Body Surface Area,
and Sodium Excretion
The black subjects were older than the white
subjects, with greater BSA (Table 1). The correlation
between age and BSA was significant (r=0.60;
p<0.01). There was a higher percentage of girls
among the black subjects and a higher percentage of
boys among the white subjects. UNaV was similar for
black and white subjects (Table 1).
Race, Sodium Excretion, and Casual Blood Pressure
The effects of both race (p<0.01) and UNaV
(/?<0.001) on casual SBP were significant. In addition, the race by UNaV interaction was significant
(/?<0.001), indicating that the slopes between UNaV
and SBP were different for black and white subjects.
The slope was positive and significant for black
subjects (/?<0.001); the slope was not significant for
white subjects (Figure 1). Further analyses were
Harshfield et al
• Black subjects
° White subjects
130-
140-1
Black
8 = 0.17
r = O57
p < 0.001
o ••%,
120-
• p<0.001
'So
X
g
1
no-
Asl
8«
90
80-
80
6
70
0
50
100
150
200
250
300
350
Sodium Excretion (mEq/24 hours)
FIGURE 1. Scatter plot shows relation between sodium
excretion and casual systolic blood pressure (SBP) for both
black and white subjects.
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performed with the inclusion of gender in the model
to control for group differences on this variable. The
race by UNaV interaction remained significant
(p<0.01). Although the effect of gender was significant (p<0.01), the interaction among race, UNaV,
and gender was not significant. Significant effects
were not found for either DBP or HR.
Race, Sodium Excretion, and Ambulatory Blood
Pressure While Awake
The effects of race, UNaV, and the interaction
between race and UNaV were not significant for SBP
while the subjects were awake. However, further analysis indicated that the slope relating UNaV to awake
SBP was positive and significant for the black subjects
(Figure 2). Similar results were obtained after the
inclusion of gender (/?=NS) in the model. Significant
effects were not found for either DBP or HR.
Race, Sodium Excretion, and Ambulatory Blood
Pressure While Asleep
The effect of UNaV on SBP while the subjects were
asleep was significant (/?<0.01). In addition, the race
150-1
• Black subjects
O White subjects
140-
is
T
° * ^ *°*
130-
(3
Black
P = 0.08
r = 0.36
p < 0.01
120White
p = 0.03
r = 0.18
p = ns
at
J<
110-
<
100-
- p < 0.03
CA
White
8 = 0.04
r = 0.18
loo-
815
• Black subjects
O White subjects
BP(mi
140
Na + and Ambulatory Blood Pressure
^ ^ 8* 2!o Vo* *
50
100
150
200
250
300
350
Sodium Excretion (mEq/24 hours)
FIGURE 2. Scatter plot shows relation between sodium
excretion and systolic blood pressure (SBP) while awake for
both black and white subjects.
50
100 150 200 250 300
Sodium Excretion (mEq/24 hours)
FIGURE 3. Scatter plot shows relation between sodium
excretion and systolic blood pressure (SBP) while asleep for
both black and white subjects.
by UNaV interaction was significant (p<0.03), indicating that the slopes between UNaV and SBP were
different for both black and white subjects. The slope
was positive and significant for black subjects
(p<0.01); the slope was not significant for white
subjects (Figure 3). The race by UNaV interaction
remained significant (/?<0.03) after the inclusion of
gender (/?=NS) in the model. Significant effects were
not found for either DBP or HR.
Race, Sodium Excretion, and Plasma Renin Activity
Both black and white subjects had similar levels of
PRA (Table 1). The slope relating PRA to UNaV was
negative for the white subjects and approached statistical significance (r=-0.22; p<0.06). PRA and
UNaV were not related for black subjects (r=0.07).
Race, Sodium Excretion, Potassium Excretion, and
Blood Pressure
Black subjects had significantly lower levels of UKV
than white subjects (Table 1). The slopes relating UNaV
to UKV were similar for black subjects ()3=1.360;
p<0.001) and for white subjects ( B= 1.662; p<0.001),
with a higher intercept for the black subjects (97.21
meq/24 hr) than for white subjects (58.8 meq/24 hr). In
addition, UKV was not related to any measure of BP
(casual, awake, or asleep) for either group.
Discussion
The increased prevalence of essential hypertension
among black adults is well documented.20 Previously,
we demonstrated that healthy normotensive black
adolescents have higher levels of BP than white
individuals at night, despite similar levels of BP
during the day.1 Furthermore, we2 and others3 demonstrated that healthy, normotensive black adults
have a smaller nocturnal decline in BP than previously observed in white adults.21-25 Based on these
observations, we hypothesized that the additional
"cardiovascular strain" resulting from the blunted
nocturnal decline in BP among black individuals may
be a contributing factor to the racial difference in the
prevalence of hypertension.2
816
Hypertension
Vol 18, No 6 December 1991
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The present study suggests that Na+ handling and
regulation contribute to the racial differences in
ambulatory BP patterns. The slopes relating UNaV to
SBP were different for both black and white subjects.
Specifically, UNaV was related to casual SBP in black
subjects, with higher levels of Na+ intake (as determined by UNaV) associated with higher levels of SBP.
Similar relations were found between UNaV and SBP
while awake and UNaV and SBP while asleep. In
contrast, UNaV was not related to SBP for white
subjects under any condition.
These findings are consistent with the only study to
our knowledge to examine the influence of Na+
intake on 24-hour BP.26 In that study, 20 healthy
subjects had 24-hour recordings performed before
and after Na+ restriction (107 versus 11 meq/24 hr).
The mesor (a "running mean") for SBP was significantly lower after the reduction in Na+ intake (115
versus 104 mm Hg). As in the present study, DBP
was not affected. It should be noted that the previous
study was performed under hospital conditions and
required the subjects to remain in a reclining position
throughout the recording.
These findings are also consistent with research
indicating that Na+ handling contributes to racial
differences in the prevalence of essential hypertension. The studies of Luft and his colleagues27 demonstrated that black subjects as a group were more
salt-sensitive (SS) than white subjects as a group. The
black subjects excreted significantly less Na+ than
white subjects the first 10 hours and 24 hours after
Na+ loading. The delayed excretion of the Na+ load
of the black subjects was associated with a greater
increase in BP. In addition, they demonstrated that a
diet of 800 meq of Na+ was needed to raise BP for
black subjects compared with a diet of 1,200 meq Na+
for white subjects, with a correlation between UNaV
and BP of 0.73 for black subjects and only 0.48 for
white subjects. Sullivan28 examined the responses of
normotensive and borderline hypertensive subjects in
response to a sodium-restricted diet and during the
return to their ad libitum diet. He found that 27% of
the black and 15% of the white normotensive subjects, as well as 50% of the black and 24% of the
white borderline hypertensive subjects were SS, defined as a 5% or greater change in mean BP from the
sodium-restricted diet to their ad libitum diet. During Na+ depletion, BP was significantly lower in the
SS than in the salt-resistant (SR) normotensive subjects. The changes observed in mean BP were paralleled by changes in forearm vascular resistance,
which was significantly higher during Na+ repletion
in the SS subjects. BP was significantly higher in the
borderline hypertensive subjects. In contrast, forearm vascular resistance was not significantly different
between the normotensive and borderline hypertensive groups, but was significantly higher in the SS
subjects. Venous capacitance was significantly lower
in the SS hypertensive than in SR hypertensive
subjects. Although a similar trend was seen in normotensive subjects, the differences were not signifi-
cant, and changes in capacitance did not accompany
changes of Na+ intake. During Na+ depletion, PRA
was significantly lower in SS than in SR subsets of
subjects and remained significantly lower even with
the added stimulus of upright posture. Plasma aldosterone concentration was also significantly lower in
the SS subjects during Na+ depletion with a significant negative correlation between the change in BP
with Na+ repletion and either PRA during Na+
restriction or the increment in PRA during Na+
depletion. Sowers and his colleagues29 examined
changes in BP from a normal Na+ diet to a low Na+
diet in two groups of black subjects: 11 hypertensive
black subjects and 14 normotensive black subjects
with a strong family history of hypertension. All of
the subjects had 5-10 mm Hg decreases in mean BP
with similar decreases for both normotensive and
hypertensive subjects. Dustan and Kirk30 reported
racial differences in BP changes in response to 3 days
each of Na+ loading and depletion with greater
changes for black subjects than white subjects. In a
study of 38 white and 83 black subjects, Falkner and
Kushner8 found that 37.3% of the black subjects
compared with 18.4% of the white subjects were SS.
Several characteristics of SS subjects have been
identified that may account for the observed differences in Na+ handling. Salt sensitivity has been
associated with altered adrenergic regulation.6-31-34
Results of these studies suggest that SS individuals
fail to adequately suppress the adrenergic system
under conditions of high Na+ intake. Other studies,
including those of Sullivan and Luft described above,
suggest that SS individuals do not regulate the reninangiotensin system appropriately in response to
changes in Na+ intake.12"16 The results of the present
study indirectly support the latter hypothesis. The
correlation between UNaV and PRA was negative and
approached significance in white subjects, suggesting
that PRA decreases in response to increases in Na+
intake. However, PRA was not associated with UNaV
in black subjects. The studies of Williams and Hollenberg16 indicate that a subset of SS subjects referred to as "non-modulators" do not alter the
responsiveness of the renal vasculature and the adrenal gland to angiotensin II in response to changes
in Na+ intake. Specifically, Na+ restriction did not
enhance adrenal responsiveness to angiotensin II35
and Na+ loading did not increase baseline renal
blood flow or renal vasculature responses to angiotensin II. In addition, these individuals showed delayed suppression of PRA after Na+ loading, coupled
with a reduction in the ability to excrete the load.36
More recent studies have demonstrated the heritability of this response pattern37 and demonstrated
that the majority of these abnormalities are corrected
by angiotensin converting enzyme inhibition.38 Other
investigators have shown that SS subjects have abnormal baroreceptor reflex function,39-40 and still
others have found a relation between sodium sensitivity and erthrocyte sodium concentration.15
Harshfield et al Na+ and Ambulatory Blood Pressure
The influence of Na+ on BP may be mediated by
K . Morgan and his colleagues910 demonstrated that
K+ supplementation prevents Na+-induced rises in
BP in people with SS hypertension. In addition,
Svetkey et al11 showed that K+ supplementation was
more effective in reducing BP in black than in white
adults with mild hypertension. In the current study,
black subjects were characterized by lower levels of
UKV. However, the slopes relating UKV to UNaV
were positive and similar for both black and white
subjects, suggesting that the influence of K+ on Na+
handling was similar. In addition, UKV was not
related to casual, awake, or asleep BP in either black
or white subjects after adjustment for body size.
In summary, the results of the current study suggest that Na+ handling is one factor responsible for
racial differences in ambulatory BP patterns in children and adolescents. Within black subjects, the
relation between UNaV and BP was positive and
linear for casual SBP, awake SBP, and asleep SBP. In
contrast, UNaV was not associated with SBP in white
subjects under any condition. UNaV was not associated with DBP or HR in either group under any
condition. Further analyses indicated these results
were not due to racial differences in UKV but were
consistent with the hypothesis that black individuals
do not adequately suppress PRA in response to
increases in Na+ intake.
Interpretation of these results must take into account the cross-sectional design of the study. Further
research is needed to determine if directly manipulating Na+ intake in black subjects will increase
awake and asleep BP but will not change BP in white
subjects. In addition, UNaV was collapsed across
24-hour periods, which did not allow us to examine
directly the relation between UNaV and BP under
each condition. Additional studies are needed to
determine if UNaV while awake is directly related to
BP while awake and if UNaV during sleep is directly
related to BP during sleep. However, the results are
consistent with the literature demonstrating the importance of Na+ on the regulation of BP for black
individuals and extends these results to BP while
awake and while asleep.
+
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Acknowledgment
We thank the staff of the Pediatric Clinical Research Center for their technical assistance.
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KEY WORDS • ambulatory blood pressure monitoring • sodium
• ethnic differences • sodium-dependent hypertension
Sodium excretion and racial differences in ambulatory blood pressure patterns.
G A Harshfield, B S Alpert, D A Pulliam, E S Willey, G W Somes and F B Stapelton
Hypertension. 1991;18:813-818
doi: 10.1161/01.HYP.18.6.813
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