Articles

Reduced Dietary Potassium Reversibly Enhances Vasopressor Response to Stress in African Americans

Krishnankutty Sudhir, Alex Forman, Sai-Li Yi, Jonathan Sorof, Olga Schmidlin, Anthony Sebastian, R. Curtis Morris
https://doi.org/10.1161/01.HYP.29.5.1083
Hypertension. 1997;29:1083-1090
Originally published May 1, 1997

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Abstract

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.

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.

Methods

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.

Results

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.

View this table:
Table 1.

Effects of Increases in Dietary Intakes of NaCl and Potassium After Their Restriction on Metabolic Variables in Normotensive Black and White Men

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).

View this table:
Table 2.

Effects of Increases in Dietary Intakes of NaCl and Potassium After Their Restriction on Blood Pressure and Forearm Vascular Resistance in Response to Cold and Mental Stresses in Normotensive Black and White Men

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.

Figure 1.
Figure 1.

Effects of increases in dietary intakes of NaCl and potassium after their restriction on changes in forearm vascular resistance (FVR), systolic pressure (ΔSBP), and diastolic pressure (ΔDBP) in response to cold in white and black normotensive men. *P<.05.

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⇑).

Figure 2.
Figure 2.

Effects of increases in dietary intakes of NaCl and potassium after their restriction on changes in forearm vascular resistance (FVR), systolic pressure (ΔSBP), and diastolic pressure (ΔDBP) in response to mental stress in white and black normotensive men. *P<.05.

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.

View this table:
Table 3.

Effect of Prolonged Dietary NaCl Loading and Potassium Restriction After NaCl Restriction on Blood Pressure and Forearm Vascular Resistance in Normotensive Blacks (Time Controls)

Discussion

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 α-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 α-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, α-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 β-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 α-adrenergic tone6 whose continued vasoconstrictive effect attenuates β-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 β-adrenergic blockade, increases more in blacks,6 as if an already enhanced α-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 α-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 β-adrenoceptor–mediated vasodilation is blunted in blacks. α-Adrenergically mediated vasoconstriction, enhanced by a reduced dietary potassium intake, could of course complement blunted β-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 β-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 α-adrenergic activity can be an important pathogenetic determinant of essential hypertension27 28 and a marginally reduced dietary intake of potassium can render the α-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.

Acknowledgments

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.

Footnotes

  • 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.
  • Revision received August 21, 1996.
  • Accepted October 29, 1996.

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  • Reduced Dietary Potassium Reversibly Enhances Vasopressor Response to Stress in African Americans
    Krishnankutty Sudhir, Alex Forman, Sai-Li Yi, Jonathan Sorof, Olga Schmidlin, Anthony Sebastian and R. Curtis Morris
    Hypertension. 1997;29:1083-1090, originally published May 1, 1997
    https://doi.org/10.1161/01.HYP.29.5.1083
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