(Hypertension. 1997;29:1083-1090.)
© 1997 American Heart Association, Inc.
Articles |
Reduced Dietary Potassium Reversibly Enhances Vasopressor Response to Stress in African Americans
From the Department of Medicine, General Clinical Research Center, University of California, San Francisco.
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Abstract |
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Abstract Acute vasopressor responses to stress are adrenergically mediated and hence potentially subject to differential modulation by dietary potassium and sodium. The greater vasopressor responsiveness in blacks compared with whites might then be consequent not only to a high dietary salt intake but also to a marginally reduced dietary potassium intake. Under controlled metabolic conditions, we compared acute vasopressor responses to cold and mental stress in black and white normotensive men during three successive dietary periods: (1) while dietary potassium was reduced (30 mmol K+/70 kg per day) and salt was restricted (10 to 14 days); (2) while salt was loaded (15 to 250 mmol Na+/70 kg per day) (7 days); and (3) while salt loading was continued and potassium was either supplemented (70 mmol K+/70 kg per day) (7 to 21 days) in 9 blacks and 6 whites or continued reduced (30 mmol K+/70 kg per day) (28 days) in 4 blacks (time controls). At the lower potassium intake, cold-induced increase in forearm vascular resistance in blacks was twice that in whites during both salt restriction and salt loading. Normalization of dietary potassium attenuated cold-induced increases in both forearm vascular resistance and systolic and diastolic blood pressures in blacks but only in systolic pressure in whites. In blacks but not in whites, normalization of dietary potassium attenuated mental stress–induced increases in systolic and diastolic pressures. In normotensive blacks but not whites, a marginally reduced dietary intake of potassium reversibly enhances adrenergically mediated vasopressor responsiveness to stress. That responsiveness so enhanced over time might contribute to the pathogenesis of hypertension in blacks.
Key Words: potassium • blacks • cold • mental stress • race
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Introduction |
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Both genetic and environmental factors may account for the greater age-specific mean blood pressure (BP) and twice greater prevalence of "essential" hypertension in African Americans (blacks) compared with Caucasian Americans (whites).1 2 In normotensive blacks, the acute increase in BP induced by experimental cold and mental stress is also greater, as is the attending and presumably causal increase in total peripheral vascular resistance (TPR), cardiac output increasing little or not at all.3 4 5 6 7 8 9 10 11 The greater vasopressor response to such sympathetic stimuli dates from childhood.8 9 11 12 13 Cardiovascular responses to stressors in the laboratory have been reported to correlate with those in the extralaboratory environment.14 15 Given the recurring environmental stress many blacks endure from childhood, their greater vasopressor response to such stress could entrain over time their greater basal or "resting" values of TPR and BP relative to whites.4 16 17 18 19 In fact, a heightened vasopressor response to sympathetic stimuli is reported to predict not only higher levels of resting BP9 20 21 but also the occurrence of hypertension.22 23 24 25 A heightened vasopressor response may be so predicting because the increased adrenergic activity that mediates it may be an important pathogenetic determinant of essential hypertension.26 27 28
Adrenergically mediated vasopressor responsiveness is subject to complex dietary modulation, varying in magnitude not only directly with the dietary intake of sodium29 30 31 32 33 but also inversely with the dietary intake of potassium.34 35 36 37 38 In epidemiological studies, BP also varies directly with dietary sodium and inversely with dietary potassium.39 40 41 42 43 44 45 46 47 Supplementing dietary potassium can attenuate hypertension48 49 50 51 52 ; restricting dietary potassium can exacerbate it.53 On average, the dietary intake of sodium in blacks approximates that in whites, but the dietary intake of potassium in blacks is substantially lower than that in whites from childhood39 40 41 42 43 54 and often is frankly reduced.55 Thus, a reduced dietary intake of potassium might contribute critically to the heightened adrenergically mediated vasopressor response observed in blacks from childhood and hence to the hypertension that response may entrain over time. Furthermore, in blacks, compared with whites, adrenergically mediated vasopressor responsiveness might be inherently more susceptible to enhancement by a given reduction in dietary potassium and to further enhancement by an increase in dietary sodium.
To test these hypotheses, we measured the effects of cold and mental stress on forearm vascular resistance (FVR) and BP in normotensive black and white men sequentially receiving (1) a low salt, marginally reduced potassium diet; (2) a high salt, marginally reduced potassium diet; and (3) a high salt, normal potassium diet.
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Methods |
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Subjects and Setting
Under controlled metabolic conditions, we conducted 19 studies on 18 normotensive healthy male volunteers confined to the General Clinical Research Center at Moffitt Hospital, University of California, San Francisco, for periods ranging from 39 to 42 days. Fifteen subjects, 9 black men (mean age, 38.1±3.2 years) and 6 white men (mean age, 41.7±3.2 years) participated in the primary study. Three additional black subjects (mean age, 42.3±5.5 years) and 1 of the 9 blacks in the primary study participated in a time control study. Subjects had no history or clinical evidence of acute or chronic disease and were on no medications. All were within 30% of their ideal body weight, as determined by Metropolitan Life Insurance Co height and weight tables. Physical activity was limited to daily walks on the one floor of the center. The study protocol was approved by the Committee on Human Research at the University of California, San Francisco, and subjects gave written, informed consent.
Diets
Throughout each study, each subject ate a constant amount of a
nutritionally adequate "basal" whole-foods diet providing, per 70
kg body wt, 15 mmol sodium, 30 mmol potassium, and 14
mmol calcium. In each subject the total number of calories provided was
determined from the estimated amount of energy required to keep body
weight constant. The diet contained as a percentage of total calories
10% protein, 45% carbohydrates, and 45% fat. Both the specific
ingredients of each meal (breakfast, lunch, dinner, and snacks at 10:30
AM and 8 PM) and the schedule of their
provision were constant throughout each study. Fluid intake was fixed
at 25 to 30 g of deionized, distilled water per kilogram body
weight during the low salt phase and 40 g during the high
salt phase.
We studied the acute vasopressor response to cold and mental stress on each of the last days of three successive periods: (1) an initial 10- to 14-day period in which the basal low sodium, low potassium diet was continued; (2) a second 7-day period in which the dietary intake of NaCl was "loaded" to 250 mmol/70 kg per day by addition of 115 mmol directly to the food provided in the basal diet and 120 mmol as capsules (6 mmol per capsule) ingested three times a day with meals; (3) a third period in which salt loading was continued and the dietary intake of potassium was supplemented to a normal amount, 70 mmol/70 kg per day, by addition of 40 mmol as potassium bicarbonate capsules (10 mmol per capsule), ingested with meals, to the basal diet containing 30 mmol K+/70 kg per day. The third period lasted 21 days in 10 subjects (5 whites and 5 blacks) and 7 days in 5 subjects (1 white and 4 blacks). As a time control for the third period (normalized dietary potassium with continued salt loading), the second period (salt loading) was continued for 28 days without supplementation of dietary potassium to a normal amount. Throughout each study, each subject took the same number of identically appearing capsules and was not informed of their contents.
Measurement of BP
On the last day of each dietary period in each subject, BP and
forearm blood flow were measured beginning at 10 AM. BP was
measured with an automated sphygmomanometer (Dinamap, Critikon Inc) on
the dominant arm with subjects supine after a 10-minute period of rest.
Baseline BPs were determined by averaging the final two of three
measurements taken at 1-minute intervals. BP responses to stressors
were measured every minute throughout their application.
Measurement of Forearm Vascular Dynamics
Forearm blood flow was measured with venous-occlusion
plethysmography (Hokanson EC-5R), as previously
described.56 Changes in forearm blood volume were
determined by means of a mercury-in-rubber strain-gauge plethysmograph
placed on the midforearm of the nondominant arm. To eliminate any
effect of the hand vessels on these measurements, a 7-cm-wide
sphygmomanometric cuff was inflated around the wrist to induce a
pressure exceeding systolic arterial pressure just
before each venous occlusion. A sphygmomanometric cuff 13 cm wide was
placed around the upper arm, and forearm venous occlusion was induced
by suddenly inflating this cuff to a constant pressure (55 mm Hg)
below the diastolic arterial pressure with the
use of a tank of compressed air. Flow was measured at baseline and in
response to the following stressors: (1) cold stimulation for 1 minute
induced by application of ice to the ipsilateral aspect of the neck,
with the assessment of the maximal reduction in blood flow during this
period; (2) mental stress for 3 minutes, induced by having the subject
perform an arithmetic task of appropriate difficulty (sequential
subtraction in sevens from 1000), with assessment of the maximal
increase in blood flow; and (3) occlusion of forearm
arterial inflow for 10 minutes, induced by ischemic
cuff occlusion, with subsequent release of the cuff and measurement of
the hyperemic response. During the application of each stress,
the maximal changes in systolic, diastolic, and
mean BPs and in heart rate were measured.
Laboratory Measurements
Body weights were measured each morning at 6 AM.
Throughout the study, spontaneously voided urine was collected over
24-hour periods and preserved with thymol. Urinary values reported are
those obtained on the last day of each dietary period. Venous blood
specimens were obtained in the morning during the fasting state on the
last day of each dietary period. Electrolytes were measured in blood
and urine with the use of standard techniques in the General Clinical
Research Center core laboratory.
Calculations and Statistical Analysis
FVR at baseline and in response to each stress was calculated
from the relationship FVR=MAP/FBF, where MAP is mean
arterial pressure and FBF is forearm blood flow. Since
baseline FVR varied with diet, results are expressed as both absolute
values and percent changes from baseline. The effects of the three
diets on changes in BP, heart rate, and FVR in response to each
stressor (cold, mental stress, ischemic cuff occlusion) were
compared within each group (blacks and whites) and between groups
(blacks versus whites) with a two-way repeated measures ANOVA followed
by a post hoc Student-Newman-Keuls test (SigmaStat, Jandel Scientific
Software, version 2.0, Jandel Corp). All data are expressed as
mean±SEM. The null hypothesis was rejected at a value of
P<.05.
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Results |
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Effect of Different Dietary Intakes of Sodium and Potassium on Metabolic Variables
Table 1
shows the effects of dietary interventions
on metabolic variables. At all three dietary intakes of
sodium and potassium, the values of the measured metabolic
variables in blacks were similar to those in whites.
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Baseline Hemodynamics
In whites, neither salt loading nor potassium supplementation
altered baseline mean arterial pressure (low NaCl/low
K+, 81±3; high NaCl/low K+, 82±5; high
NaCl/normal K+, 82±3 mm Hg), heart rate (low
NaCl/low K+, 69±4; high NaCl/low K+, 68±3;
high NaCl/normal K+, 64±4 beats per minute), or FVR (see
Table 2). However, in black subjects, there was a rise
in mean arterial pressure from the low NaCl/low potassium
diet to the high NaCl/low potassium diet (83±2 to 88±2 mm Hg,
P<.05) that was sustained during the high NaCl/normal
potassium diet (87±2 mm Hg). FVR decreased in blacks from the
low NaCl/low potassium to the high NaCl/low potassium diet
(P<.05) but rose again during the high NaCl/normal
potassium diet (Table 2, P<.05). In blacks, as in whites,
heart rate did not change between diets (low NaCl/low K+,
68±2; high NaCl/low K+, 68±2; high NaCl/normal
K+, 72±3 beats per minute). Maximal forearm circumference
was greater in black than white subjects (28.4±0.2 versus 26.8±0.4
cm, P=.001).
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Responses to Cold Stimulation
There was a significant race-by-diet interaction with respect to
FVR responses to cold, indicating that the effect of diet on these
responses differed in blacks and whites. In the low potassium/low NaCl
period, the magnitude of the FVR response to cold in blacks was
significantly greater that in whites and remained so after the FVR
response to cold increased in both during the second period, when salt
loading was imposed on the low potassium diet (Fig 1, Table 2
). When dietary intake of potassium was restricted, the
cold-induced increase in systolic and diastolic
pressures was not altered by the salt loading of period 2. However,
normalization of dietary potassium (over a period of either 7 or 21
days) significantly attenuated the cold-induced increase in FVR and
both systolic and diastolic pressures in blacks and
diastolic pressure in whites, despite continued salt
loading (Fig 1). Diet did not alter heart rate changes in response to
cold in either racial group.
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SBP), and
diastolic pressure (
Responses to Mental Stress
Despite reduced dietary potassium, salt loading did not augment
the increase in systolic and diastolic BPs induced
by mental stress in either blacks or whites. In blacks but not whites,
normalization of dietary potassium (over a period of either 7 or 21
days) did attenuate the increase in both systolic and
diastolic BPs induced by mental stress and despite
continued salt loading (Fig 2). Diet did not alter the
heart rate response to mental stress in either racial group. As with
cold, there was a significant race-by-diet interaction with respect to
FVR responses to mental stress, indicating that the effect of diet on
these responses differed in blacks and whites. In white subjects, FVR
decreased substantially (49±9%) in response to mental stress in the
low NaCl/low potassium period. FVR decreased less when salt was loaded
(31±10%) and when dietary potassium was normalized (24±8%). By
contrast, in black subjects in response to mental stress, FVR decreased
to only 18±5% during the low NaCl/low potassium period, to 37±7%
during the high NaCl/low potassium period, and to 13±6% during the
high NaCl/normal potassium period (Fig 2, Table 2).
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Hyperemic Response to Ischemic Cuff
Occlusion
After ischemic cuff occlusion was released during the low
NaCl/low potassium period, forearm blood flow was higher (33.4±1.6
versus 25.8±4.3 mL/100 mL per minute, P=.07) and FVR
significantly lower in blacks than whites (2.6±1.4 versus
3.7±0.5 mm Hg/mL per 100 mL per minute, P=.026). Salt
loading and potassium supplementation did not have any significant
effects on the hyperemic response in either blacks or
whites.
Time Controls
To address the question of whether potassium-induced attenuation
of vasopressor responses to stress might be due to familiarization with
the circumstances of the study resulting from repeated testing, we
studied four time controls. In these time controls, the attenuation of
vasopressor responses to stressors observed when dietary intake of
potassium was normalized did not occur when, over a comparable time
period, dietary potassium remained reduced and salt intake remained
increased (Table 3). In one subject studied twice, the
vasopressor response to cold remained unchanged when salt loading was
continued without normalization of dietary potassium.
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Discussion |
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The current results demonstrate that the acute vasopressor response to cold and mental stress of normotensive black men but not that of normotensive white men is strikingly susceptible to modulation by dietary potassium over a range of intake extending from only a marginally reduced to a midnormal value (30 to 70 mmol/d). At the reduced intake of potassium, the cold-induced increase in FVR of the blacks was significantly greater than that of the whites both during salt restriction and after salt loading had augmented the increase in both groups. Yet despite continued salt loading, increasing the dietary intake of potassium to only a midnormal value significantly reduced the cold-induced increase in FVR in the blacks but not in the whites. In the blacks but not in the whites, normalization of dietary potassium significantly attenuated the otherwise large increase in both systolic and diastolic BPs induced by mental stress at the lower dietary intake of potassium. Normalization of the dietary intake of potassium abolished both the cold-induced increase in systolic and diastolic BPs in the blacks and the systolic increase in the whites. In the aggregate, these observations suggest that in blacks, the vasopressor response to sympathetic stress is reversibly enhanced by a marginally reduced intake of potassium.
In the present study, increasing the dietary intake of potassium from 30 to 70 mmol/d induced a slight increase in the serum concentration of potassium in both blacks and whites, but at neither intake was the serum concentration or urinary excretion of potassium of blacks different from that of whites. Thus, at neither intake can the differing vasopressor responsiveness observed in blacks and whites be attributed to different plasma concentrations or intestinal absorptions of potassium. Accordingly, the results of the current study suggest that the greater acute vasopressor responsiveness to cold reported in blacks reflects both their usually reduced intake of potassium39 40 41 42 43 54 55 and a greater acute vasopressor responsiveness to it. Of particular note, the marginally reduced dietary intake of potassium used in the current study, 30 mmol/d, constitutes a potassium restriction so modest that serum potassium concentrations remained well within the normal range in both blacks and whites, with and without salt loading. By contrast, in previous studies38 57 in which dietary potassium restriction was attended by an increase in resting BP, frank hypokalemia occurred, either because the dietary restriction of potassium was much more severe (10 mmol/d for 10 days57 ) or was combined with massive salt loading (400 mmol/d for 6 days38 ). In those studies, blacks were not studied, and vasopressor responses to cold and mental stress were not examined.
Potassium-induced natriuresis58 59 might explain the attenuation of vasopressor responses to adrenergic stress observed in blacks in the present study. However, the observed differences in vasopressor responsiveness between blacks and whites during potassium supplementation in the current study cannot be attributed to a differential natriuresis because the magnitude of the increase in daily and cumulative sodium excretion during the period of potassium supplementation was not statistically greater in blacks in our study than in whites. It is of course possible that enhanced vasopressor responsiveness in blacks is a consequence of greater, although undetected, sodium retention, as described by Luft et al,60 or reflects a greater sensitivity to changes in the body content of sodium than in whites.
The vasopressor response to cold is mediated in large part by increased
-adrenergic activity61 62 that evokes
peripheral vasoconstriction and thereby an increase in
arterial BP.63 64 Cold stimulates an increase
in sympathetic neural outflow to the skeletal muscle vasculature (as
recorded in the peroneal nerve).65 The cold-induced
increase in neural outflow so recorded has recently been reported
to be greater in blacks than whites and associated with greater
concomitant increases in both systolic and
diastolic BPs.10 Although this observation
probably reflects an enhanced sympathetic nervous response to cold in
blacks, differences in blacks and whites in their somatosensory
perception of cold cannot be excluded. In normotensive and hypertensive
white men,38 a short-term dietary restriction of potassium
that induced hypokalemia did not affect peroneal nerve activity but did
induce an increase both in ambulatory BP and in the BP rise occurring
with acute orthostasis, a potent -adrenergic
stimulus.66 Conversely, supplementation of dietary
potassium has been found to attenuate not only the acute
orthostatic increase in BP in salt-sensitive hypertensive
individuals, with and without salt restriction,35 but also
the pressor response to intravenously administered
norepinephrine in both hypertensive white
subjects37 and their normotensive first-order
relatives.34 37 The pressor response to
intravenously administered norepinephrine, and
its amplification by dietary salt loading, was found to be greater in
blacks than whites in metabolically controlled studies in
which the urinary excretion of potassium in blacks remained marginally
low and substantially less than that of whites despite both having
received the same generous dietary intake of potassium (100 mmol/d
for 5 days).67 Thus, in the blacks compared with whites, a
relative and habitual deficiency of potassium might have been a
critical determinant of their greater pressor response to exogenous
norepinephrine. The current observation that the
vasoconstrictive response to cold was greater in blacks
than whites, but only at the reduced intake of potassium, might
indicate then that in blacks, -adrenoceptor responsiveness to
endogenous norepinephrine is especially
susceptible to enhancement by moderate reductions in potassium
intake.
The cardiovascular response to psychological stress is
mediated in large part by increased ß-adrenergic
activity68 69 that evokes an increase in cardiac output
and decrease in TPR, the latter reflected by an increase in forearm
blood flow. However, it has been proposed that in blacks, the mental
stress–induced increase in BP is amplified by a preexisting enhanced
-adrenergic tone6 whose continued
vasoconstrictive effect attenuates ß-adrenergically
mediated peripheral vasodilation. This proposal is based on
the observation that in response to mental stress, TPR is greater in
blacks than whites and, after pharmacological ß-adrenergic blockade,
increases more in blacks,6 as if an already enhanced
-adrenergic tone then operates unopposed. Thus, in the current
study, as with cold-induced vasoconstriction (see above), normalization
of dietary potassium might have attenuated the pressor response to
mental stress only in blacks by dampening an otherwise enhanced
-adrenergic tone. In fact, the mental stress–induced forearm
vasodilation was significantly less in blacks than whites when assessed
during the lower dietary intakes of potassium and salt.
Having observed that isoproterenol administered into the brachial
artery induced a lesser forearm vasodilation in blacks than whites,
Lang et al70 recently concluded that
ß-adrenoceptor–mediated vasodilation is blunted in blacks.
-Adrenergically mediated vasoconstriction, enhanced by a reduced
dietary potassium intake, could of course complement blunted
ß-adrenergically mediated vasodilation in effecting enhanced
sympathetically mediated vasoconstriction in blacks. It has been
suggested that this kind of adrenergic complementarity may occur in
hypertension.71 72 In the present study, when salt
loading was superimposed on the low potassium intake, the mental
stress–induced increase in forearm blood flow increased further in
blacks whereas it decreased in whites. Salt loading is reported to
enhance responsiveness to the ß-adrenergic agonist isoproterenol in
blacks but diminish this response in whites.73
Whereas the dietary intakes of salt and potassium were systematically manipulated in the present study, other dietary components and physical activity were fixed. Whether different diets and levels of physical activity can modify the vasopressor responses to dietary manipulation of potassium and salt remains to be determined. It happened that the normotensive black subjects in the current study were all salt sensitive, whereas none of the normotensive white subjects were salt sensitive—a difference reflecting the fact that salt sensitivity is quite common in normotensive black men and much less so in normotensive white men.74 75 76 77 It is possible that studies in blacks who are not salt sensitive might yield different results. The observation in the current study that the hyperemic response was greater in the blacks than the whites contrasts with a previously reported observation78 and might relate to the greater forearm circumference in the black subjects we studied.
If enhanced -adrenergic activity can be an important pathogenetic
determinant of essential hypertension27 28 and a
marginally reduced dietary intake of potassium can render the
-adrenergic system in blacks especially susceptible to amplification
by sympathetic stressors, a marginally reduced dietary intake of
potassium might increase the likelihood of the occurrence of
hypertension in young normotensive black men.
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Acknowledgments |
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These studies were carried out in the General Clinical Research Center, University of California, San Francisco, with funds provided by the Division of Research Resources, 5 MO1 RR-000079, US Public Health Service, the National Heart, Lung, and Blood Institute (RO1 HL-47943), and generous gifts from the Church and Dwight Corp and the Emil Mosbacher, Jr, Foundation.
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Footnotes |
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Reprint requests to R. Curtis Morris Jr, MD, General Clinical Research Center, University of California at San Francisco, 1202 Moffitt Hospital, Box 0126, San Francisco, CA 94143-0126.
Received August 5, 1996; first decision August 21, 1996; accepted October 29, 1996.
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