Skip to main content
  • American Heart Association
  • Science Volunteer
  • Warning Signs
  • Advanced Search
  • Donate

  • Home
  • About this Journal
    • General Statistics
    • Editorial Board
    • Editors
    • Information for Advertisers
    • Author Reprints
    • Commercial Reprints
    • Customer Service and Ordering Information
  • All Issues
  • Subjects
    • All Subjects
    • Arrhythmia and Electrophysiology
    • Basic, Translational, and Clinical Research
    • Critical Care and Resuscitation
    • Epidemiology, Lifestyle, and Prevention
    • Genetics
    • Heart Failure and Cardiac Disease
    • Hypertension
    • Imaging and Diagnostic Testing
    • Intervention, Surgery, Transplantation
    • Quality and Outcomes
    • Stroke
    • Vascular Disease
  • Browse Features
    • AHA Guidelines and Statements
    • Acknowledgment of Reviewers
    • Clinical Implications
    • Clinical-Pathological Conferences
    • Controversies in Hypertension
    • Editors' Picks
    • Guidelines Debate
    • Meeting Abstracts
    • Recent Advances in Hypertension
    • SPRINT Trial: the Conversation Continues
  • Resources
    • Instructions to Reviewers
    • Instructions for Authors
    • →Article Types
    • → Submission Guidelines
      • Research Guidelines
        • Minimum Information About Microarray Data Experiments (MIAME)
      • Abstract
      • Acknowledgments
      • Clinical Implications (Only by invitation)
      • Conflict(s) of Interest/Disclosure(s) Statement
      • Figure Legends
      • Figures
      • Novelty and Significance: 1) What Is New, 2) What Is Relevant?
      • References
      • Sources of Funding
      • Tables
      • Text
      • Title Page
      • Online/Data Supplement
    • →Tips for Easier Manuscript Submission
    • → General Instructions for Revised Manuscripts
      • Change of Authorship Form
    • → Costs to Authors
    • → Open Access, Repositories, & Author Rights Q&A
    • Permissions to Reprint Figures and Tables
    • Journal Policies
    • Scientific Councils
    • AHA Journals RSS Feeds
    • International Users
    • AHA Newsroom
  • AHA Journals
    • AHA Journals Home
    • Arteriosclerosis, Thrombosis, and Vascular Biology (ATVB)
    • Circulation
    • → Circ: Arrhythmia and Electrophysiology
    • → Circ: Genomic and Precision Medicine
    • → Circ: Cardiovascular Imaging
    • → Circ: Cardiovascular Interventions
    • → Circ: Cardiovascular Quality & Outcomes
    • → Circ: Heart Failure
    • Circulation Research
    • Hypertension
    • Stroke
    • Journal of the American Heart Association
  • Facebook
  • Twitter

  • My alerts
  • Sign In
  • Join

  • Advanced search

Header Publisher Menu

  • American Heart Association
  • Science Volunteer
  • Warning Signs
  • Advanced Search
  • Donate

Hypertension

  • My alerts
  • Sign In
  • Join

  • Facebook
  • Twitter
  • Home
  • About this Journal
    • General Statistics
    • Editorial Board
    • Editors
    • Information for Advertisers
    • Author Reprints
    • Commercial Reprints
    • Customer Service and Ordering Information
  • All Issues
  • Subjects
    • All Subjects
    • Arrhythmia and Electrophysiology
    • Basic, Translational, and Clinical Research
    • Critical Care and Resuscitation
    • Epidemiology, Lifestyle, and Prevention
    • Genetics
    • Heart Failure and Cardiac Disease
    • Hypertension
    • Imaging and Diagnostic Testing
    • Intervention, Surgery, Transplantation
    • Quality and Outcomes
    • Stroke
    • Vascular Disease
  • Browse Features
    • AHA Guidelines and Statements
    • Acknowledgment of Reviewers
    • Clinical Implications
    • Clinical-Pathological Conferences
    • Controversies in Hypertension
    • Editors' Picks
    • Guidelines Debate
    • Meeting Abstracts
    • Recent Advances in Hypertension
    • SPRINT Trial: the Conversation Continues
  • Resources
    • Instructions to Reviewers
    • Instructions for Authors
    • →Article Types
    • → Submission Guidelines
    • →Tips for Easier Manuscript Submission
    • → General Instructions for Revised Manuscripts
    • → Costs to Authors
    • → Open Access, Repositories, & Author Rights Q&A
    • Permissions to Reprint Figures and Tables
    • Journal Policies
    • Scientific Councils
    • AHA Journals RSS Feeds
    • International Users
    • AHA Newsroom
  • AHA Journals
    • AHA Journals Home
    • Arteriosclerosis, Thrombosis, and Vascular Biology (ATVB)
    • Circulation
    • → Circ: Arrhythmia and Electrophysiology
    • → Circ: Genomic and Precision Medicine
    • → Circ: Cardiovascular Imaging
    • → Circ: Cardiovascular Interventions
    • → Circ: Cardiovascular Quality & Outcomes
    • → Circ: Heart Failure
    • Circulation Research
    • Hypertension
    • Stroke
    • Journal of the American Heart Association
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
Krishnankutty Sudhir
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Alex Forman
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Sai-Li Yi
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Jonathan Sorof
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Olga Schmidlin
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Anthony Sebastian
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
R. Curtis Morris
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • Article
  • Figures & Tables
  • Info & Metrics
  • eLetters

Jump to

  • Article
    • Abstract
    • Methods
    • Results
    • Discussion
    • Acknowledgments
    • Footnotes
    • References
  • Figures & Tables
  • Info & Metrics
  • eLetters
Loading

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.

  • potassium
  • blacks
  • cold
  • mental stress
  • race

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:
  • View inline
  • View popup
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:
  • View inline
  • View popup
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.
  • Download figure
  • Open in new tab
  • Download powerpoint
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.
  • Download figure
  • Open in new tab
  • Download powerpoint
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:
  • View inline
  • View popup
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.

References

  1. ↵
    Roberts J, Maurer K. National Center for Health Statistics: blood pressure levels of persons 6-74 years, United States, 1971-1974. In: Vital and Health Statistics. Washington, DC: US Government Printing Office; 1977:1-103. US Dept of Health, Education, and Welfare publication HRA 78-1648, series 11, No. 203.
  2. ↵
    Report of the Task Force on Black and Minority Health, Executive Summary, Volume 1. Washington, DC: US Government Printing Office; 1985. Dept of Health and Human Services publication 86-52P.
  3. ↵
    Light KC, Obrist PA, Sherwood A, James SA, Strogatz DS. Effects of race and marginally elevated blood pressure on responses to stress. Hypertension. 1987;10:555-563.
    OpenUrlAbstract/FREE Full Text
  4. ↵
    Thomas J, Semenya K, Thomas CB, Thomas DJ, Neser WB, Pearson TA, Gillum RF. Precursors of hypertension in black compared to white medical students. J Chronic Dis. 1987;40:721-727.
    OpenUrlCrossRefPubMed
  5. ↵
    Anderson NB, Lane JD, Muranaka M, Williams RBJ, Houseworth SJ. Racial differences in blood pressure and forearm vascular responses to the cold face stimulus. Psychosom Med. 1988;50:57-63.
    OpenUrlAbstract/FREE Full Text
  6. ↵
    Light KC, Sherwood A. Race, borderline hypertension, and hemodynamic responses to behavioral stress before and after beta-adrenergic blockade. Health Psychol. 1989;8:577-595.
    OpenUrlCrossRefPubMed
  7. ↵
    McAdoo WG, Weinberger MH, Miller JZ, Fineberg NS, Grim CE. Race and gender influence hemodynamic responses to psychological and physical stimuli. J Hypertens. 1990;8:961-967.
    OpenUrlCrossRefPubMed
  8. ↵
    Treiber FA, Musante L, Braden D, Arensman F, Strong WB, Levy M, Leverett S. Racial differences in hemodynamic responses to the cold face stimulus in children and adults. Psychosom Med. 1990;52:286-296.
    OpenUrlAbstract/FREE Full Text
  9. ↵
    Murphy JK, Alpert BS, Walker SS. Ethnicity, pressor reactivity, and children’s blood pressure: five years of observations. Hypertension. 1992;20:327-332.
    OpenUrlAbstract/FREE Full Text
  10. ↵
    Calhoun DA, Mutinga ML, Collins AS, Wyss JM, Oparil S. Normotensive blacks have heightened sympathetic response to cold pressor test. Hypertension. 1993;22:801-805.
    OpenUrlAbstract/FREE Full Text
  11. ↵
    Dysart JM, Treiber FA, Pflieger K, Davis H, Strong WB. Ethnic differences in the myocardial and vascular reactivity to stress in normotensive girls. Am J Hypertens. 1994;7:15-22.
    OpenUrlAbstract/FREE Full Text
  12. ↵
    Voors AW, Webber LS, Berenson GS. Racial contrasts in cardiovascular response tests for children from a total community. Hypertension. 1980;2:686-694.
    OpenUrlAbstract/FREE Full Text
  13. ↵
    Alpert BS, Fox ME. Racial aspects of blood pressure in children and adolescents. Pediatr Clin North Am. 1993;40:13-22.
    OpenUrlPubMed
  14. ↵
    Dimsdale JE, Mills P, Dillon E. Does reactivity testing in the laboratory reflect blood pressure changes elsewhere? J Psychosom Med. 1992;36:701-705.
    OpenUrlCrossRef
  15. ↵
    Matthews KA, Owens JF, Allen MT, Stoney CM. Do cardiovascular responses to laboratory stress relate to ambulatory blood pressure levels? Yes, in some of the people, some of the time. Psychosom Med. 1992;54:686-697.
    OpenUrlAbstract/FREE Full Text
  16. ↵
    Falkner B. Is there a black hypertension? Hypertension. 1987;10:551-554.
    OpenUrlFREE Full Text
  17. ↵
    Arensman FW, Treiber FA, Gruber MP, Strong WB. Exercise-induced differences in cardiac output, blood pressure, and systemic vascular resistance in a healthy biracial population of 10-year-old boys. Am J Dis Child. 1989;143:212-216.
    OpenUrlCrossRefPubMed
  18. ↵
    Soto LF, Kikuchi DA, Arcilla RA, Savage DD, Berenson GS. Echocardiographic functions and blood pressure levels in children and young adults from a biracial population: the Bogalusa Heart Study. Am J Med Sci. 1989;297:271-279.
    OpenUrlPubMed
  19. ↵
    Savage DD, Watkins LO, Grim CE, Kumanyika SK. Hypertension in black populations. In: Laragh JH, Brenner BM, eds. Hypertension: Pathophysiology, Diagnosis, and Management. New York, NY: Raven Press Publishers; 1990:1837-1852.
  20. ↵
    Parker FC, Croft JB, Cresanta JL, Freedman DS, Burke GL, Webber LS, Berenson GS. The association between cardiovascular response tasks and future blood pressure levels in children: Bogalusa Heart Study. Am Heart J. 1987;113:1174-1179.
    OpenUrlCrossRefPubMed
  21. ↵
    Matthews KA, Woodall KL, Allen MT. Cardiovascular reactivity to stress predicts future blood pressure status. Hypertension. 1993;22:479-485.
    OpenUrlAbstract/FREE Full Text
  22. ↵
    Falkner B, Kushner H, Onesti G, Angelakos ET. Cardiovascular characteristics in adolescents who develop essential hypertension. Hypertension. 1981;3:521-527.
    OpenUrlAbstract/FREE Full Text
  23. ↵
    Wood DL, Sheps SG, Elveback LR, Schirger A. Cold pressor test as a predictor of hypertension. Hypertension. 1984;6:301-306.
    OpenUrlAbstract/FREE Full Text
  24. ↵
    Borghi C, Costa FV, Boschi S, Mussi A, Ambrosioni E. Predictors of stable hypertension in young borderline subjects: a five-year follow-up study. J Cardiovasc Pharmacol. 1986;8:S138-S141.
    OpenUrl
  25. ↵
    Menkes MS, Matthews KA, Krantz DS, Lundberg U, Mead LA, Qaqish B, Liang K-Y, Thomas CB, Pearson TA. Cardiovascular reactivity to the cold pressor test as a predictor of hypertension. Hypertension. 1989;14:524-530.
    OpenUrlAbstract/FREE Full Text
  26. ↵
    Hollenberg NK, Adams DF, Solomon H, Chenitz WR, Burger BM, Abrams HL, Merrill JP. Renal vascular tone in essential and secondary hypertension: hemodynamic and angiographic responses to vasodilators. Medicine. 1975;54:29-44.
    OpenUrlCrossRefPubMed
  27. ↵
    Egan B, Panis R, Hinderliter A, Schork N, Julius S. Mechanism of increased alpha adrenergic vasoconstriction in human essential hypertension. J Clin Invest. 1987;80:812-817.
  28. ↵
    Esler M, Ferrier C, Lambert G, Eisenhofer G, Cox H, Jennings G. Biochemical evidence of sympathetic hyperactivity in human hypertension. Hypertension. 1991;17(suppl III):III-29-III-35.
  29. ↵
    Rankin LI, Luft FC, Henry DP, Gibbs PS, Weinberger MD. Sodium intake alters the effect of norepinephrine on blood pressure. Hypertension. 1981;3:650-656.
    OpenUrlAbstract/FREE Full Text
  30. ↵
    Ambrosioni E, Costa FV, Borghi C, Montebugnoli L, Giordani MF, Magnani B. Effects of moderate salt restriction on intralymphocytic sodium and pressor response to stress in borderline hypertension. Hypertension. 1982;4:789-794.
    OpenUrlAbstract/FREE Full Text
  31. ↵
    Skrabal F, Herholz H, Neumayr M, Hamberger L, Ledochowski M, Sporer H, Hortnagl H, Schwarz S, Schonitzer D. Salt sensitivity in humans is linked to enhanced sympathetic responsiveness and to enhanced proximal tubular reabsorption. Hypertension. 1984;6:152-158.
    OpenUrlPubMed
  32. ↵
    Dimsdale JE, Graham RM, Ziegler MG, Zusman RM, Berry CC. Age, race, diagnosis, and sodium effects on the pressor response to infused norepinephrine. Hypertension. 1987;10:564-569.
    OpenUrlAbstract/FREE Full Text
  33. ↵
    Sharma AM, Schattenfroh S, Thiede H, Oelkers W, Distler A. Effects of sodium salts on pressor reactivity in salt-sensitive men. Hypertension. 1992;19:541-548.
    OpenUrlPubMed
  34. ↵
    Skrabal F, Aubock J, Hortnagl H. Low sodium/high potassium diet for prevention of hypertension: probable mechanisms of action. Lancet. 1981;2:895-900.
    OpenUrlPubMed
  35. ↵
    Morgan T, Teow BH, Myers J. The role of potassium in control of blood pressure. Drugs Ther Perspect. 1984;28:188-195.
    OpenUrl
  36. ↵
    Dietz R, Schomig A, Dart AM, Mayer E, Kubler W. Modulation of sympathetic vasoconstriction by potassium. J Cardiovasc Pharmacol. 1984;6:S230-S235.
  37. ↵
    Bianchetti MG, Weidmann P, Beretta-Piccoli C, Ferrier C. Potassium and norepinephrine- or angiotensin-mediated pressor control in pre-hypertension. Kidney Int. 1987;31:956-963.
    OpenUrlPubMed
  38. ↵
    Lawton WJ, Fitz AE, Anderson EA, Sinkey CA, Coleman RA. Effect of dietary potassium on blood pressure, renal function, muscle sympathetic nerve activity, and forearm vascular resistance and flow in normotensive and borderline hypertensive humans. Circulation. 1990;81:173-184.
    OpenUrlAbstract/FREE Full Text
  39. ↵
    Berenson GS, Voors AW, Dalferes ER Jr, Webber LS, Shuler SE. Creatinine clearance, electrolytes, and plasma renin activity related to the blood pressure of white and black children: the Bogalusa Heart Study. J Lab Clin Med. 1979;93:535-548.
    OpenUrlPubMed
  40. ↵
    Grim CE, Luft FC, Miller JZ, Meneely GR, Battarbee HD, Hames CG, Dahl LK. Racial differences in blood pressure in Evans County, Georgia: relationship to sodium and potassium intake and plasma renin activity. J Chronic Dis. 1980;33:87-94.
    OpenUrlCrossRefPubMed
  41. ↵
    Watson RL, Langford HG. Weight, urinary electrolytes and blood pressure: results of several community based studies. J Chronic Dis. 1982;35:909-918.
    OpenUrlCrossRefPubMed
  42. ↵
    Frisancho AR, Leonard WR, Bollettino LA. Blood pressure in blacks and whites and its relationship to dietary sodium and potassium intake. J Chronic Dis. 1984;37:515-519.
    OpenUrlCrossRefPubMed
  43. ↵
    Talmers FN, Cushman WC, Schnaper H, White TJ, Hla KM, Fernandez O, Ramirez EA, Khatri I. Urinary and serum electrolytes in untreated black and white hypertensives. J Chronic Dis. 1987;40:839-847.
    OpenUrlCrossRefPubMed
  44. ↵
    Khaw K, Barrett-Connor E. The association between blood pressure, age, and dietary sodium and potassium: a population study. Circulation. 1988;77:53-61.
    OpenUrlAbstract/FREE Full Text
  45. ↵
    Elliott P, Dyer A, Stamler R, INTERSALT Co-operative Research Group. The INTERSALT study: results for 24 hour sodium and potassium, by age and sex. J Hum Hypertens. 1989;3:323-330.
    OpenUrlPubMed
  46. ↵
    Khaw K, Barrett-Connor E. Increasing sensitivity of blood pressure to dietary sodium and potassium with increasing age: a population study using casual urine specimens. Am J Hypertens. 1990;3:505-511.
    OpenUrlPubMed
  47. ↵
    Geleijnse JM, Grobbee DE, Hofman A. Sodium and potassium intake and blood pressure change in childhood. Br Med J. 1990;300:899-902.
  48. ↵
    MacGregor GA, Markandu ND, Smith SJ, Banks RA, Sagnella GA. Moderate potassium supplementation in essential hypertension. Lancet. 1982;2:567-570.
    OpenUrlPubMed
  49. ↵
    Siani A, Strazzullo P, Russo L, Guglielmi S, Iacoviello L, Ferrara LA, Mancini M. Controlled trial of long term oral potassium supplements in patients with mild hypertension. Br Med J. 1987;294:1453-1456.
  50. ↵
    Svetkey LP, Yarger WE, Feussner JR, DeLong E, Klotman PE. Double-blind, placebo-controlled trial of potassium chloride in the treatment of mild hypertension. Hypertension. 1987;9:444-450.
    OpenUrlAbstract/FREE Full Text
  51. ↵
    Obel AO. Placebo-controlled trial of potassium supplements in black patients with mild essential hypertension. J Cardiovasc Pharmacol. 1989;14:294-296.
    OpenUrlPubMed
  52. ↵
    Patki PS, Singh J, Gokhale SV, Bulakh PM, Shrotri DS, Patwardhan B. Efficacy of potassium and magnesium in essential hypertension: a double blind, placebo controlled, crossover study. Br J Med. 1990;301:521-523.
    OpenUrl
  53. ↵
    Krishna GG, Kapoor SC. Potassium depletion exacerbates essential hypertension. Ann Intern Med. 1991;115:77-83.
  54. ↵
    Zemel P, Gualdoni S, Sowers JR. Racial differences in mineral intake in ambulatory normotensives and hypertensives. Am J Hypertens. 1988;1:146S-148S.
    OpenUrlPubMed
  55. ↵
    Food and Nutrition Board, National Research Council, Havel RJ, Calloway DH, Gussow JD, Mertz W, Nesheim MC. Water and electrolytes. In: Recommended Dietary Allowances. 10th ed. Washington, DC: National Academy Press; 1989:247-261.
  56. ↵
    Panza JA, Quyyumi AA, Brush JEJ, Epstein SE. Abnormal endothelium-dependent vascular relaxation in patients with essential hypertension. N Engl J Med. 1990;323:22-27.
    OpenUrlCrossRefPubMed
  57. ↵
    Krishna GG, Miller E, Kapoor S. Increased blood pressure during potassium depletion in normotensive men. N Engl J Med. 1989;320:1177-1182.
    OpenUrlCrossRefPubMed
  58. ↵
    Keith NM, Binger MW. Diuretic action of potassium salts. JAMA. 1935;105:1584-1591.
    OpenUrlCrossRef
  59. ↵
    Van Buren M, Rabelink TJ, Van Rijn HJM, Koomans HA. Effects of acute NaCl, KCl and KHCO3 loads on renal electrolyte excretion in humans. Clin Sci. 1992;83:567-574.
    OpenUrlPubMed
  60. ↵
    Luft FC, Rankin LI, Bloch R, Weyman AE, Willis LR, Murray RH, Grim CE, Weinberger MH. Cardiovascular and humoral responses to extremes of sodium intake in normal black and white men. Circulation. 1979;60:697-706.
    OpenUrlFREE Full Text
  61. ↵
    Abboud FM, Eckstein JW. Active reflex vasodilation in man. Fed Proc. 1966;25:1611-1617.
    OpenUrlPubMed
  62. ↵
    Abboud FM, Eckstein JW. Reflex vasoconstrictor and vasodilator responses in man. Circ Res. 1966;18,19(suppl I):I-96-I-103.
  63. ↵
    Ayman D, Goldshine AR. Cold as a standard stimulus of blood pressure: a study of normal and hypertensive subjects. N Engl J Med. 1938;219:650-655.
    OpenUrl
  64. ↵
    Miller JH, Bruger M. The cold-pressor reaction in normal subjects and in patients with primary (essential) and secondary (renal) hypertension. Am Heart J. 1939;18:329-333.
    OpenUrlCrossRef
  65. ↵
    Victor RG, Leimbach WN, Seals DR, Wallin BG, Mark AL. Effects of the cold pressor test on muscle sympathetic nerve activity in humans. Hypertension. 1987;9:429-436.
    OpenUrlAbstract/FREE Full Text
  66. ↵
    Robertson D, Johnson GA, Robertson RM, Nies AS, Shand DG, Oates JA. Comparative assessment of stimuli that release neuronal and adrenomedullary catecholamines in man. Circulation. 1979;59:637-643.
    OpenUrlAbstract/FREE Full Text
  67. ↵
    Dimsdale JE, Ziegler M, Mills P, Berry C. Prediction of salt sensitivity. Am J Hypertens. 1990;3:429-435.
    OpenUrlPubMed
  68. ↵
    Eisenhofer G, Lambie DG, Johnson RH. B-adrenoceptor responsiveness and plasma catecholamines as determinants of cardiovascular reactivity to mental stress. Clin Sci. 1985;69:483-492.
    OpenUrlPubMed
  69. ↵
    Mills PJ, Dimsdale JE, Ziegler MG, Berry CC, Bain RD. Beta-adrenergic receptors predict heart rate reactivity to a psychosocial stressor. Psychosom Med. 1990;52:621-623.
    OpenUrlAbstract/FREE Full Text
  70. ↵
    Lang CC, Stein CM, Brown RM, Deegan R, Nelson R, He HB, Wood M, Wood HJJ. Attenuation of isoproterenol-mediated vasodilatation in blacks. N Engl J Med. 1995;333:155-160.
    OpenUrlCrossRefPubMed
  71. ↵
    Hollister AS, Onrot J, Lonce S, Nadeau JHJ, Robertson D. Plasma catecholamine modulation of alpha2 adrenoceptor agonist affinity and sensitivity in normotensive and hypertensive human platelets. J Clin Invest. 1986;77:1416-1421.
  72. ↵
    Feldman RD. Defective venous beta-adrenergic responses in borderline hypertensive subjects is corrected by a low sodium diet. J Clin Invest. 1990;85:647-652.
  73. ↵
    Dimsdale J, Ziegler M. The effect of hypertension, sodium, and race on isoproterenol sensitivity. Clin Exp Hypertens A. 1988;10:747-756.
    OpenUrlPubMed
  74. ↵
    Luft FC, Grim CE, Fineberg N, Weinberger MC. Effects of volume expansion and contraction in normotensive whites, blacks, and subjects of different ages. Circulation. 1979;59:643-650.
    OpenUrlAbstract/FREE Full Text
  75. ↵
    Sullivan JM, Prewitt RL, Ratts TE. Sodium sensitivity in normotensive and borderline hypertensive humans. Am J Med Sci. 1988;295:370-377.
    OpenUrlCrossRefPubMed
  76. ↵
    Sowers JR, Zemel MB, Zemel P, Beck FWJ, Walsh MF, Zawada ET. Salt sensitivity in blacks: salt intake and natriuretic substances. Hypertension. 1988;12:485-490.
    OpenUrlAbstract/FREE Full Text
  77. ↵
    Falkner B, Kushner H. Effect of chronic sodium loading on cardiovascular response in young blacks and whites. Hypertension. 1990;15:36-43.
    OpenUrlAbstract/FREE Full Text
  78. ↵
    Bassett DR Jr, Duey WJ, Walder AJ, Howley ET, Bond V. Racial differences in maximal vasodilatory capacity of forearm resistance vessels in normotensive young adults. Am J Hypertens. 1992;5:781-786.
    OpenUrlAbstract/FREE Full Text
View Abstract
Back to top
Previous ArticleNext Article

This Issue

Hypertension
May 1997, Volume 29, Issue 5
  • Table of Contents
Previous ArticleNext Article

Jump to

  • Article
    • Abstract
    • Methods
    • Results
    • Discussion
    • Acknowledgments
    • Footnotes
    • References
  • Figures & Tables
  • Info & Metrics
  • eLetters

Article Tools

  • Print
  • Citation Tools
    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

    Citation Manager Formats

    • BibTeX
    • Bookends
    • EasyBib
    • EndNote (tagged)
    • EndNote 8 (xml)
    • Medlars
    • Mendeley
    • Papers
    • RefWorks Tagged
    • Ref Manager
    • RIS
    • Zotero
  •  Download Powerpoint
  • Article Alerts
    Log in to Email Alerts with your email address.
  • Save to my folders

Share this Article

  • Email

    Thank you for your interest in spreading the word on Hypertension.

    NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address.

    Enter multiple addresses on separate lines or separate them with commas.
    Reduced Dietary Potassium Reversibly Enhances Vasopressor Response to Stress in African Americans
    (Your Name) has sent you a message from Hypertension
    (Your Name) thought you would like to see the Hypertension web site.
  • Share on Social Media
    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
    del.icio.us logo Digg logo Reddit logo Twitter logo CiteULike logo Facebook logo Google logo Mendeley logo

Related Articles

Cited By...

Hypertension

  • About Hypertension
  • Instructions for Authors
  • AHA CME
  • Guidelines and Statements
  • Permissions
  • Journal Policies
  • Email Alerts
  • Open Access Information
  • AHA Journals RSS
  • AHA Newsroom

Editorial Office Address:
7272 Greenville Ave.
Dallas, TX 75231
email: hypertension@heart.org

Information for:
  • Advertisers
  • Subscribers
  • Subscriber Help
  • Institutions / Librarians
  • Institutional Subscriptions FAQ
  • International Users
American Heart Association Learn and Live
National Center
7272 Greenville Ave.
Dallas, TX 75231

Customer Service

  • 1-800-AHA-USA-1
  • 1-800-242-8721
  • Local Info
  • Contact Us

About Us

Our mission is to build healthier lives, free of cardiovascular diseases and stroke. That single purpose drives all we do. The need for our work is beyond question. Find Out More about the American Heart Association

  • Careers
  • SHOP
  • Latest Heart and Stroke News
  • AHA/ASA Media Newsroom

Our Sites

  • American Heart Association
  • American Stroke Association
  • For Professionals
  • More Sites

Take Action

  • Advocate
  • Donate
  • Planned Giving
  • Volunteer

Online Communities

  • AFib Support
  • Garden Community
  • Patient Support Network
  • Professional Online Network

Follow Us:

  • Follow Circulation on Twitter
  • Visit Circulation on Facebook
  • Follow Circulation on Google Plus
  • Follow Circulation on Instagram
  • Follow Circulation on Pinterest
  • Follow Circulation on YouTube
  • Rss Feeds
  • Privacy Policy
  • Copyright
  • Ethics Policy
  • Conflict of Interest Policy
  • Linking Policy
  • Diversity
  • Careers

©2018 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. The American Heart Association is a qualified 501(c)(3) tax-exempt organization.
*Red Dress™ DHHS, Go Red™ AHA; National Wear Red Day ® is a registered trademark.

  • PUTTING PATIENTS FIRST National Health Council Standards of Excellence Certification Program
  • BBB Accredited Charity
  • Comodo Secured