Published online before print November 11, 2002, doi: 10.1161/01.HYP.0000041417.94797.57
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(Hypertension. 2002;40:914.)
© 2002 American Heart Association, Inc.
Scientific Contributions |
Reactivity as a Predictor of Subsequent Blood Pressure
Racial Differences in the Coronary Artery Risk Development in Young Adults (CARDIA) Study
From the Division of Epidemiology and Clinical Applications, National Heart, Lung, and Blood Institute (S.S.K.), Bethesda, Md; Harvard Medical School (J.H.), Boston, Mass; and the Division on Aging, Department of Medicine, University of Alabama at Birmingham (J.H.M.).
Correspondence to Sarah S. Knox, PhD, National Heart, Lung, and Blood Institute, II Rockledge Center, 6701 Rockledge Dr, Room 8120, Bethesda, MD 20892. E-mail knoxs{at}nhlbi.nih.gov
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Abstract |
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This study investigated the association between cardiovascular reactivity and subsequent ambulatory blood pressure in 316 black and white men and women in the Coronary Artery Risk Development in Young Adults (CARDIA) Study. Cardiovascular laboratory reactivity was examined in subjects 20 to 33 years old, and ambulatory blood pressure and heart rate were measured 3 years later. Average ambulatory pressure during a 24-hour period was regressed separately on stress reactivity and standard covariate risk factors in each race/gender subgroup. Blacks had higher blood pressure and heart rates than whites, men had higher blood pressure than women, and women had higher heart rates than men. After controlling for age, baseline systolic pressure, familial history of hypertension, smoking, alcohol consumption, body mass index, and exercise, systolic blood pressure reactivity to star tracing and cold pressor stress were significantly associated with systolic ambulatory pressure in black men and women 3 years later (partial r=0.24 to 0.37). Heart rate reactivity to video challenge and star tracing were also significantly predictive of subsequent ambulatory heart rate in blacks. Diastolic star tracing reactivity was significantly associated with subsequent ambulatory blood pressure in black women (r=0.23), and diastolic reactivity to video and star tracing were significantly predictive of ambulatory diastolic pressure in white men (r=0.39). We conclude that hyperresponsivity to stress may be a risk factor for subsequent blood pressure elevation in blacks and may be one pathway leading to the higher prevalence of hypertension in blacks than in whites.
Key Words: blood pressure • race • stress
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Introduction |
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Blood pressure responsiveness to mental stress has been reported to be a significant predictor of exercise-induced myocardial ischemia1 and carotid artery atherosclerosis.2 Although it has also been reported to predict stable hypertension in borderline-hypertensive individuals,3 its utility as a prognostic measure has been questioned,4 and data concerning the association between stress reactivity and ambulatory blood pressure have been equivocal.5–11 A number of these studies are difficult to interpret because they were either based solely on correlations, only examined absolute levels during reactivity, or did not control for relevant covariates.12–15 There has been little research examining the effect of race and gender on the association between reactivity and subsequent ambulatory pressure, despite the fact that previous research has been fairly consistent in showing race as well as gender differences in reactivity and blood pressure measured at a single sitting.16–19
The goal of the present study was to investigate whether cardiovascular reactivity to mental stress predicted subsequent ambulatory blood pressure differently in race/gender subgroups. Ambulatory blood pressure was chosen because it better reflects blood pressure variation and levels throughout the day than clinical measurements made at a single point in time.20 A second objective was to test whether previously reported higher nighttime blood pressure in blacks21 would be verified in a young, healthy cohort.
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Methods |
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The Coronary Artery Risk Development in Young Adults Study (CARDIA) is an ongoing, prospective, epidemiologic study, conducted at four sites. A detailed description of the study design and recruitment methods can be found in an earlier publication.22 The data presented in this report are from a substudy conducted at one site, Birmingham, Alabama. The protocol was approved by the institutional review board, procedures followed were in accordance with institutional guidelines, and informed consent was obtained from each participant.
Subjects
Because of the high cost and time-consuming nature of cardiovascular reactivity testing and ambulatory blood pressure monitoring, these measurements were performed only at only one site, Birmingham. The reactivity testing was performed in the second examination year, 1987, when the subjects were 20 to 33 years old. Ambulatory blood pressure monitoring was performed at the subsequent examination, in 1990, when the median age was 30 (range, 23 to 36 years old). A list of 400 Alabama participants consisting of 100 individuals randomly selected from each of the four race/gender subgroups (black and white men and women) was generated at the CARDIA Coordinating Center. Partially because of the reluctance of already-burdened healthy participants to submitting to yet another long procedure, and partially because of the nature of certain types of employment (delivery people, truck drivers, and so forth, who could not stop and stretch their arms every 20 minutes for ambulatory measurements), it was not possible to recruit all 400 people. The total sample size was 316 (147 men and 169 women). There were 204 blacks (88 men and 116 women) and 112 whites (59 men and 53 women).
Procedure
Reactivity Testing
The procedure for reactivity testing has been described in detail elsewhere.23 There were three tasks: a video game (Atari Breakout, Atari Corporation), a mirror star-tracing task, and a cold pressor task (immersion of hand into ice water). The 8-minute baseline period was followed by 3-minute video and star-tracing tasks (order was randomized). The 45- to 60-second cold pressor task was performed last because of the long recovery time. The time interval between tasks was 2 minutes. Reactivity was defined as mean blood pressure or heart rate during stress task minus average during baseline.
Ambulatory Monitoring
Ambulatory blood pressure and heart rate were monitored for 24 hours with a Suntech Accutracker II, which was inflated approximately every 20 minutes. The inflation schedule was variable, to reduce the effects of anticipation. If any value outside preset limits (>220 or <80 mm Hg, systolic; and >130 or <40 mm Hg, diastolic) was detected during a recording, a rejection code was given for that measurement and another measurement was immediately made. In addition, a change of 50 mm Hg in systolic pressure, of 40 mm Hg in diastolic pressure, or of 50 mm Hg in pulse pressure also triggered a rejection code and a new reading.
Blood pressure dipping was defined as the difference between average daytime pressure and the average nighttime pressure.
Statistical Methods
To isolate the effects of blood pressure reactivity from other factors that are known to influence blood pressure levels, analyses were calculated by regressing ambulatory blood pressure on blood pressure reactivity, controlling for average blood pressure during an 8-minute baseline habituation period; smoking status (smoker, nonsmoker, ex-smoker); familial history of hypertension in one or both parents; alcohol consumption (self-report) in milliliters per day; body mass index (BMI); and physical activity score calculated from the total combined intensity of sports, exercise, home maintenance work, and physical activity at work.24
This cohort was young, and their average 24-hour ambulatory pressure was low (115/68 mm/Hg). There were only 4 people whose mean overall systolic pressure exceeded 140 mm/Hg. Analyses were calculated in time segments as well as for the entire 24-hour period. The segments analyzed were morning (7 AM to noon), afternoon (1 to 6 PM), evening (6 PM to midnight), and night (1 to 6 AM). The nighttime hours were chosen for biological reasons, to achieve an average sleep pressure.
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Results |
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Race/Gender Differences in Ambulatory Pressure
Because ambulatory pressure was not measured at the examination in which the reactivity testing was done, the baseline measures for blood pressure at the reactivity examination consist of the average of 4 resting baseline measures. These results can be seen in Table 1. ANOVA revealed no significant race differences in blood pressure or heart rate; however, the race differences in ambulatory systolic pressure showed a tendency toward significance (P<0.06). Black and white men did not differ significantly, but white women had significantly lower pressure than all three groups, accounting for most of the borderline significance.
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A comparison of mean ambulatory blood pressure by race and gender at different times of the day, 3 years later, can be seen in Tables 2 and 3.
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Blacks had higher overall systolic and diastolic blood pressure and heart rate than whites and higher pressure during each of the separate periods of the day. These differences were all significant except for diastolic blood pressure and heart rate in the morning. There were also significant gender differences in blood pressure, which were consistent across time periods with the exception of morning diastolic pressure. Men had significantly higher mean systolic and diastolic pressures than women. With respect to heart rate, blacks had higher average ambulatory heart rate than whites (82 versus 79 beats per minutes, P<0.02).
Laboratory Reactivity as a Predictor of Subsequent Ambulatory Pressure and Heart Rate
After controlling for age, baseline systolic pressure, familial history of hypertension, BMI, physical activity, smoking status, alcohol consumption, and eliminating the persons receiving antihypertensive medication, star tracing and cold pressor systolic reactivity in black men and women were significantly associated with mean overall systolic ambulatory blood pressure 3 years later. There were no significant associations between systolic reactivity and subsequent systolic ambulatory pressure in whites. With respect to diastolic pressure, reactivity to star tracing was significantly associated with overall diastolic ambulatory pressure in black women, and diastolic reactivity to video and star tracing was significantly associated with subsequent ambulatory pressure in white men. These results can be seen in Tables 4 and 5.
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After controlling for baseline heart rate and other covariates, video and star tracing heart rate reactivity in the laboratory were significantly associated with subsequent ambulatory heart rate in black men and women only. These results can be seen in Table 6.
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Because an earlier CARDIA report on the full cohort reported that baseline heart rate was a predictor of hypertension across 5 examinations, average ambulatory pressure at examination 3 was regressed on baseline heart rate at examination 2, adjusting for examination 2 blood pressure, as was done in the earlier analyses. There were no significances, probably because of the limited range of time.
Dipping was defined as average daytime pressure minus nighttime pressure. There were no racial differences in nighttime dipping of blood pressure.
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Discussion |
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The use of ambulatory blood pressure monitoring has increased steadily with increasing evidence that blood pressure measured in a single session has limited generalizability to average daytime levels,25 and with the knowledge that ambulatory measures are more closely correlated with cardiovascular risk than multiple office blood pressure measurements.26–28 The rationale for investigating cardiovascular reactivity in relation to subsequent ambulatory pressure is the long-standing hypothesis that if an individual has an increased magnitude of response in stressful situations, and this type of response occurs fairly often, secondary vascular changes in the form of an increase in wall-to-lumen ratio in hypertensive resistance vessels will occur,29,30 causing an increase in peripheral resistance accompanied by permanent blood pressure elevation. This is called the "recurrent activation model."31 In support of this theory, it has been shown in a follow-up study lasting 45 to 57 years32 that blood pressure reactivity to cold pressor stress, one of the tasks investigated in the current study, is a strong predictor of subsequent hypertension. Based on these data, the fact that blacks in our study were more reactive to cold pressor than whites would suggest that they may be more likely to have hypertension. However, controlled investigations of reactivity with the use of animal models have demonstrated that the associations are not linear33 and that high blood pressure reactors do not get hypertension without the addition of other genetic or environmental factors. Isolating influences of single factors on blood pressure is far more difficult to do in humans because not all factors influencing blood pressure can be experimentally controlled. The aim of the present study was simply to isolate the effects of cardiovascular reactivity as much as possible from parental history of hypertension and health-related behaviors that influence blood pressure, so that the association between reactivity and subsequent blood pressure could be measured independent of these influences. In addition to controlling for baseline blood pressure, age, and parental history, we adjusted for smoking, physical activity, and alcohol consumption. Dietary data were not collected at the ambulatory pressure examination, so BMI was used as the best proxy for energy intake and expenditure.
Because blood pressure regulation occurs at several levels,34 for example, in the central nervous system, at the bulbar level and locally (eg, heart, resistance vessels), pressure elevation can be, and usually is, a result of multiple interacting factors involving genes, biological factors, and environmental influences. Even though identification of hypertension genotypes has not progressed to the point of enabling investigations of environmental interactions with a specific genotype, the characterization of phenotypes is progressing. The Tecumseh Study reported that a subgroup of 37% of its borderline hypertensives had hyperkinetic circulation, displaying high sympathetic arousal characterized by increased heart rate, cardiac index, forearm blood flow and plasma norepinephrine.35 A hyperkinetic phenotype would be consistent with a larger magnitude of response to laboratory stress. Unfortunately, the Tecumseh study did not identify subjects by race or gender, making it impossible to know whether racial differences existed. Even though the current study controlled for parental history of hypertension, we could not control for parental genotype, or even parental phenotype, and our results still beg the question. What we have shown is that racial differences exist and appear to be independent of relevant health related behaviors and parental history of hypertension. Whether the racial differences were due to genotype, hyperalertness resulting from more frequently occurring stress, or a combination of gene/environment interactions cannot be answered and will have to await future studies.
With respect to the association between blood pressure reactivity and hypertension, one perspective has been that enhanced blood pressure reactivity may be an indication, rather than a predictor of hypertension, since it has been observed independent of increased heart rate reactivity.31 This is supported by rat models of hypertension, which have shown that early elevations in heart rate36 and relatively high stress-induced increases in heart rate37 are a general distinguishing characteristic of animals at high risk for hypertension. Our results show that though the average blood pressure of both groups was normal, ambulatory heart rate and blood pressure were higher in blacks than in whites, and blacks showed more consistent associations between blood pressure and heart rate responsivity and subsequent ambulatory measures than whites. This combination would be consistent with the hyperkinetic phenotype described in Tecumseh. In that study, hyperreactors at 32 years of age had normal blood pressure as children and young adults38 but elevated childhood heart rates,39 indicating that increased heart rate preceded the elevated blood pressure. Moreover, in CARDIA, an earlier study analyzing the entire cohort reported that baseline heart rate (clinic measurement) was an independent predictor of subsequent diastolic blood pressure (clinic measurements) across 5 examination periods in whites and in black men. Although heart rate did not predict blood pressure in the subset analyzed in the current study, this may have been due to the diminished time frame (3 years instead of 10 in the earlier study). The fact that ambulatory heart rate was higher and blood pressure reactivity more predictive in blacks may indicate an "at-risk" hyperkinetic phenotype. This hyperkinetic interpretation is further supported by earlier work showing that normotensive blacks had higher pressor response and total sympathetic nerve activity to the cold pressor test than whites.40
Because the limited range of blood pressure in this cohort actually reduces power to detect associations, and power is further reduced by the number of covariates in the equations, small but true differences could have gone undetected. However, these facts also suggest that the significant results that were found probably are robust and reflect true differences. The young age of CARDIA participants and the prospective design of the study have the advantage of providing a unique opportunity for identifying risk factors before the emergence of manifest disease. The fact that these analyses also controlled for baseline blood pressure, parental history of hypertension, and health-related behaviors raises the possibility that enhanced cardiovascular reactivity to acute stress has an independent association with subsequent blood pressure and may be a risk factor for hypertension in blacks.
Although it has earlier been reported that blacks demonstrated less blood pressure dipping than whites,41 those results were not replicated in the current study. This may be due to the fact that racial differences in dipping are partially mediated by parental status, which was controlled for in the present analyses,41 or it may also be that one measure of nighttime dipping is not a reliable reflection of nighttime blood pressure. A small study of 21 individuals who were monitored twice with ambulatory blood pressure, showed little test-retest reliability across the two settings with respect to nighttime dipping.42 In the current study, only one night was available for analysis, raising the question of whether the measure was reliable.
There are two limitations to the present results. One is that heart rate was measured as a pulse rather than with chest electrodes, both during reactivity testing and ambulatory monitoring. The second is that the rest periods between reactivity tasks were only 3 minutes long, meaning that recovery time may have been insufficient.23 However, the latter caveat may actually have made the stressors more similar to real-life situations (eg, a stressful workday) than a protocol allowing long, restful recovery between tasks. In any event, to the extent that this caused bias, it was the same for all groups, meaning that the stronger association of reactivity with subsequent ambulatory pressure in blacks, particularly black women, is still a meaningful distinction. Whether these differences are indicative of greater vulnerability to specific environmental stressors in blacks than in whites or whether the association occurs in conjunction with more frequently occurring or sustained stress cannot be answered by the data presented in this study but warrants further investigation.
Perspectives
Although average ambulatory pressure in both blacks and whites in this young adult cohort was within the normal range, systolic and heart reactivity to laboratory stressors were more predictive of subsequent ambulatory measures in blacks than in whites. These results were independent of resting measures of blood pressure, age, parental history of hypertension, physical activity, smoking, alcohol consumption, and body mass index. Because average blood pressure was normal but heart rate was higher in blacks than in whites, we interpret the hyperreactivity to acute stress as a precursor rather than result of elevated blood pressure. Seen in the context of other findings, these results may indicate that blacks in this study had a hyperkinetic phenotype. Future studies of gene/environment interactions are needed to elucidate this issue.
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Acknowledgments |
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This study was supported by contracts N01-HC-48047 through -48050 and N01-HC-95095 from the National Heart, Lung, and Blood Institute, National Institutes of Health.
Received May 16, 2002; first decision June 10, 2002; accepted September 30, 2002.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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1. Kral BG, Becker LC, Blumenthal RS, Aversano T, Fleisher LA, Yook RM, Becker DM. Exaggerated reactivity to mental stress is associated with exercise-induced myocardial ischemia in an asymptomatic high-risk population. Circulation. 1997; 96: 4246–4253.
2. Kamarck TW, Everson SA, Kaplan GA, Manuck SB, Jenings R, Salonen R, Salonen JT. Exaggerated blood pressure responses during mental stress are associated with enhanced carotid atherosclerosis in middle-aged Finnish men: findings from the Kuopio Ischemic Heart Disease Study. Circulation. 1997; 96: 3842–3848.
3. Borghi C, Costa FV, Boschi S, Bacchelli S, Esposti D, Piccoli M, Ambrosioni E. Factors associated with the development of stable hypertension in young borderline hypertensives. J Hypertens. 1996; 14: 509–517.[Medline] [Order article via Infotrieve]
4. Carroll D, Smith GD, Shipley MJ, Steptoe A, Brunner EJ, Marmot MG. Blood pressure reactions to acute psychological stress and future blood pressure status: a 10-year follow-up of men in the Whitehall II Study. Psychosom Med. 2001; 63: 737–743.
5. Steptoe A, Cropley M, Joekes K. Task demands and the pressures of everyday life: associations between cardiovascular reactivity and work blood pressure and heart rate. Health Psychol. 2000; 19: 46–54.[CrossRef][Medline] [Order article via Infotrieve]
6. Meininger JC, Liehr P, Mueller WH, Chan W, Smith GL, Portman RJ. Stress-induced alterations of blood pressure and 24 h ambulatory blood pressure in adolescents. Blood Press Monit. 1999; 4: 115–120.[Medline] [Order article via Infotrieve]
7. Fredrikson M, Robson A, Ljungdell T. Ambulatory and laboratory blood pressure in individuals with negative and positive family history of hypertension. Health Psychol. 1991; 10: 371–377.[CrossRef][Medline] [Order article via Infotrieve]
8. Georgiades A, Lemne C, de Faire U, Lindvall K, Fredrikson M. Stress-induced laboratory blood pressure in relation to ambulatory blood pressure and left ventricular mass among borderline hypertensive and normotensive men. Hypertension. 1996; 28: 641–646.
9. Guasti L, Diolisi A, Gaudio G, Grimoldi P, Petrozzino R, Uslenghi S, Bertolini A, Grandi AM, Venco A. Reactivity of blood pressure to mental arithmetic stress test, stress-test recovery time, and ambulatory blood pressure in hypertensive and normotensive subjects. Blood Press Monit. 1998; 3: 275–280.[Medline] [Order article via Infotrieve]
10. Seibt R, Boucsein W, Scheuch K. Effects of different stress settings on cardiovascular parameters and their relationship to daily life blood pressure in normotensives, borderline hypertensives and hypertensives. Ergonomics. 1998; 41: 634–648.[Medline] [Order article via Infotrieve]
11. Harshfield GA, James GD, Schlussel Y, Yee LS, Blank SG, Pickering TG. Do laboratory tests of blood pressure reactivity predict blood pressure changes during everyday life? Am J Hypertens. 1988; 1: 168–174.[Medline] [Order article via Infotrieve]
12. Langewitz W, Ruddel H, Schachinger H, Schmieder R. Standardized stress testing in the cardiovascular laboratory: has it any bearing on ambulatory blood pressure values? J Hypertens Suppl. 1989; 7: S41–S48.[CrossRef][Medline] [Order article via Infotrieve]
13. Turner JR, Girdler SS, Sherwood A, Light KC. Cardiovascular responses to behavioral stressors: laboratory-field generalization and inter-task consistency. J Psychosom Res. 1990; 34: 581–589.[CrossRef][Medline] [Order article via Infotrieve]
14. Cornish PJ, Blanchard EB, Jaccard J. The relationship between 24-hour ambulatory blood pressures and laboratory measures of cardiovascular reactivity. Biofeedback Self Regul. 1994; 19: 193–209.[CrossRef][Medline] [Order article via Infotrieve]
15. Linden W, Con A. Laboratory reactivity models as predictors of ambulatory blood pressure and heart rate. J Psychosom Res. 1994; 38: 217–228.[CrossRef][Medline] [Order article via Infotrieve]
16. Sherwood A, Hinderliter AL. Responsiveness to alpha- and beta-adrenergic receptor agonists: effects of race in borderline hypertensive compared to normotensive men. Am J Hypertens. 1993; 6: 630–635.[Medline] [Order article via Infotrieve]
17. Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Bethesda, Md: National Institutes of Health; 1997. Publication No. 98-4080.
18. Light KC, Turner JR, Hinderliter AL, Sherwood A. Race and gender comparisons, I: hemodynamic responses to a series of stressors. Health Psychol. 1993; 12: 354–365.[CrossRef][Medline] [Order article via Infotrieve]
19. Saab PG, Llabre MM, Schneiderman N, Hurwitz BE, McDonald PG, Evans J, Wohlgemuth W, Hayashi P, Klein B. Influence of ethnicity and gender on cardiovascular responses to active coping and inhibitory-passive coping challenges. Psychosom Med. 1997; 59: 434–446.
20. Van Boxtel MPJ, Gaillard C, van Es PN, Jolles J, de Leeuw PW. Repeated automatic versus ambulatory blood pressure measurement: the effects of age and sex in a normal aging population. J Hypertens. 1996; 14: 31–40.[Medline] [Order article via Infotrieve]
21. Profant J, Dimsdale JE. Race and diurnal blood pressure patterns: a review and meta-analysis. Hypertension. 1999; 33: 1099–1094.
22. Friedman GD, Cutter GR, Donahue RP, Hughes GH, Hulley SB, Jacobs DR Jr, Liu K, Savage PJ. CARDIA: study design, recruitment, and some characteristics of the examined subjects. J Clin Epidemiol. 1988; 41: 1105–1116.[CrossRef][Medline] [Order article via Infotrieve]
23. Markovitz JH, Raczynski JM, Wallace D, Chettur V, Chesney MA. Cardiovascular reactivity to video game predicts subsequent blood pressure increases in young men: the CARDIA Study. Psychosom Med. 1998; 60: 186–191.
24. Sidney S, Jacobs DR, Haskell WL, Armstrong MA, Dimicco A, Oberman A, Savage PJ, Slattery ML, Sternfeld B, Van Horn L. Comparison of two methods of assessing physical activity in the coronary artery risk development in young adults (CARDIA) Study. Am J Epidemiol. 1991; 133: 1231–1244.
25. Van Boxtel MPJ, Gaillard C, van Es PN, Jellemer J, de Leeuw PW. Repeated automatic versus ambulatory blood pressure measurement: the effects of age and sex in a normal ageing population. J Hypertens. 1996; 14: 31–40.[Medline] [Order article via Infotrieve]
26. Prisant LM. Ambulatory blood pressure monitoring: test reproducibility and its implications. Blood Press Monit. 1998; 3: 221–225.[Medline] [Order article via Infotrieve]
27. Turner ST, Bielak LF, Narayana AK, Sheedy PF 2nd, Schwarztz GL, Peyser PA. Ambulatory blood pressure and coronary artery calcification in middle-aged and younger adults. Am J Hypertens. 2002; 15: 518–524.[CrossRef][Medline] [Order article via Infotrieve]
28. Imai Y. Prognostic significance of ambulatory blood pressure. Blood Press Monit. 1999; 4: 249–256.[Medline] [Order article via Infotrieve]
29. Folkow B. Physiological aspects of primary hypertension. Physiol Rev. 1982; 62: 347–503.
30. Julius S. Sympathetic hyperactivity and coronary risk in hypertension. Hypertension. 1993; 21: 886–893.
31. Pickering TG, Gerin W. Area review: Blood pressure reactivity: cardiovascular reactivity in the laboratory and the role of behavioral factors in hypertension: A critical review. Ann Behav Med. 1990; 12: 3–16.[CrossRef]
32. Wood DL, Sheps SG, Elveback LR. Cold pressor test as a predictor of hypertension. Hypertension. 1984; 6: 301–306.
33. Light KC. Hypertension and the reactivity hypothesis: the next generation. Psychosom Med. 2001; 63: 744–746.
34. Folkow B. Psychosocial and central nervous influences in primary hypertension. Circulation. 1987; 76: 1–10.
35. Julius S, Krause L, Schork NJ, Mejia AD, Jones KA, van de Ven C, Johnson EJ, Sekkarie MA, Kjeldsen SE, Peterin J, Schmouder R, Gupta R, Ferraro J, Nazzaro P, Weissfeld J. Hyperkinetic borderline hypertension in Tecumseh, Michigan. J Hypertens. 1991; 9: 77–84.[Medline] [Order article via Infotrieve]
36. Dickhout JG, Lee RM. Blood pressure and heart rate development in young spontaneously hypertensive rats. Am J Physiol. 1998; 274: H794–H800.[Medline] [Order article via Infotrieve]
37. Friedman R, McCann M, Leder R. Genetic predisposition to hypertension and stress-induced alterations in heart rate. Behav Neurol Biol. 1982; 35: 426–431.[CrossRef][Medline] [Order article via Infotrieve]
38. Julius S, Jones K, Schork N, Johnson E, Krause L, Nazzaro P, Zemva A. Independence of pressure reactivity from pressure levels in Tecumseh, Michigan. Hypertension. 1991; 17 (suppl III): III-12–III-21.[Medline] [Order article via Infotrieve]
39. Julius S, Jamerson K. Sympathetics, insulin resistance and coronary risk in hypertension: the "chicken and egg" question. J Hypertens. 1994; 12: 495–502.[Medline] [Order article via Infotrieve]
40. Calhoun DA, Muthoka LM, Collins AS, Wyss M, Oparil S. Normotensive blacks have heightened sympathetic response to cold pressor test. Hypertension. 1993; 22: 801–805.
41. Ituarte PH, Kamarck TW, Thompson HS, Bacanu S. Psychosocial mediators of racial differences in nighttime blood pressure dipping among normotensive adults. Health Psychol. 1999; 18: 393–402.[CrossRef][Medline] [Order article via Infotrieve]
42. Dimsdale JE, Heeren MM. How reliable is nighttime blood pressure dipping? Am J Hypertens. 1998; 1: 606–609.
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