Cardiovascular Reactivity

Definition and Background

The cardiovascular system functions to provide nutrients to systemic tissue beds of the body, as well as to remove waste products of cellular metabolism. In order to accomplish this formidable responsibility, the heart and vasculature must work in concert and be flexible enough to respond to a wide range of activities, ranging from quiet rest or sleep to maximal exercise. Thus, the cardiovascular system is continuously "reactive," depending on the metabolic needs of the organism.

The use of the term "cardiovascular reactivity" by researchers in the field of cardiovascular behavioral medicine or psychophysiology generally is defined more narrowly than that described in the previous paragraph. That is, cardiovascular reactivity is usually understood to reflect the physiologic changes from a resting or baseline state to some type of psychological or physical challenge or stressor (Manuck et al., 1989). Importantly, it is widely thought that individuals showing exaggerated cardiovascular responses to these stressful conditions may be more at risk for the development of cardiovascular syndromes such as hypertension or coronary heart disease than those exhibiting relatively smaller responses (Manuck & Krantz, 1986). It should be pointed out that how one defines "exaggerated responses" has ranged from simply taking individuals who show the largest responses in their study group, to more rigorous attempts to define reactors in terms on whether the cardiovascular responses exceed the metabolic demands of the situation (Sherwood et al., 1986). Regardless, the underlying assumption is that large increases in cardiovascular responses to stressors that occur frequently may lead to alterations in either the heart or vasculature that can have deleterious effects on the individual’s health.

A number of epidemiological studies have pointed to an inverse relationship between SES and health outcomes; that is, lower SES is associated with increased risk for a number of diseases (see Chesney, 1996; Salonen, 1982). This relationship has also been found for SES and cardiovascular disease (see Marmot & Feeney, 1996; Siegrist et al., 1986). Although multiple factors such as diet, compliance and access to health care have been postulated, a popular conceptualization of the mechanisms linking SES and health outcomes is based upon the observations that individuals from low SES environments generally experience more day-to-day stress than individuals living in more affluent locales. This differential stress exposure along the SES gradient has implications for how one might view reactivity as either a moderator or mediator of the relationship between SES and health outcomes.

If cardiovascular reactivity during stress is a consistent physiological characteristic of an individual, then one might expect that highly reactive individuals who live in high stress environments would have a greater stress load (more frequent and greater physiological stress responses) than individuals who are either not highly reactive or live in lower stress areas. In this case, one could conceptualize reactivity as interacting with or moderating the effects of environmental stress as a link between SES and health outcomes. Another possibility for the role of reactivity as a link between SES and health outcomes is that exposure to a more threatening or challenging environment by lower SES individuals results in greater reactivity in various organ systems in response to this exposure. Over time, individuals who are chronically exposed to more threatening environments may also begin to anticipate or expect threats even in benign situations, leading to greater overall stress load on manifold organ systems. Here, reactivity plays more of a mediating role between SES/stress exposure and health outcomes. These two possibilities are not mutually exclusive; both could operate to some extent in different individuals. This summary will address both of these possibilities in later sections. Let us first turn our attention to the measurement of cardiovascular reactivity.

How one chooses to measure cardiovascular reactivity is a complex issue due to a number of potential cardiovascular variables, as well as a variety of ways in which to measure change.

Among the cardiovascular measures that have been utilized in reactivity studies are heart rate, blood pressure (systolic, diastolic, mean arterial), stroke volume (average amount of blood pumped from the left ventricle on a given contraction of the heart), cardiac output (volume of blood pumped per minute), total peripheral resistance (resistance to blood flow by the systemic vasculature - a derived measure computed when cardiac output and mean arterial pressure are known), and timing intervals in the cardiac cycle that reflect cardiac performance such as pre-ejection period (PEP) and left ventricular ejection time (LVET). Over the years, the journal Psychophysiology has published methodological guidelines for measuring heart rate, blood pressure, and impedance cardiography (a noninvasive technique for measuring stroke volume, cardiac output, total peripheral resistance, and systolic time intervals). The reader is referred to these papers for detailed discussions of measurement procedures for these cardiovascular variables.

Although not always explicitly stated, many reactivity studies are interested in how the autonomic nervous system responds to environmental challenges, and the resultant effects on the cardiovascular system. For example, heart rate reflects both sympathetic and parasympathetic (vagal) influences on the sino-atrial node, whereas PEP is most directly influenced by sympathetic influences on contractility of the ventricles of the heart. Systolic blood pressure reflects both increases in contractility of the ventricles and the amount of systemic resistance to blood flow, whereas diastolic pressure is more reflective of vascular resistance (as is of course total peripheral resistance). The variability of heart rate has also become a popular measure, as the variability of beat-to-beat heart periods may reflect the degree of vagal control of the heart under certain conditions (e.g., Porges, 1995). A number of computational procedures to measure heart rate variability have been utilized such as spectral analysis and sequential differencing techniques (Hayano et al., 1991). Thus, studies of cardiovascular reactivity to stress not only allow for examination of cardiovascular dynamics, but also give a window for assessing autonomic nervous system adjustments to these environmental demands.

Although the measurement of reactivity as reflecting the degree of change from a baseline period to some period of challenge seems simple enough, there is disagreement concerning the best way to measure "change." This disagreement often stems from how to interpret the amount of change exhibited by groups when their base rates are different. Some have championed the use of simple or raw change, whereas others have called for the use of "residualized" change scores which are computed from regression analyses of baseline and task levels. A detailed discussion of these issues is beyond the scope of this summary; the reader is referred to Wainer (1991) and Maxwell et al. (1985) for interesting observations on these issues.

It has become increasingly clear to researchers that the use of only one or two cardiovascular measures often gives an incomplete picture of autonomic adjustments that occur during laboratory challenges or everyday life. An emerging strategy is to measure a number of cardiovascular variables to examine the pattern of responses. That is, rather than look at the response of a number of variables independently, it is recognized that the cardiovascular system responds with a limited number of organized patterns of response. Remember that the cardiovascular system has a very specific and important job: to get the appropriate amount of blood flow to various vascular beds according their needs. The various measures of cardiovascular function would not be expected to vary randomly among each other, but be organized in a finite number of patterns that respond to various environmental demands. Individuals are therefore studied based upon their composite pattern of autonomic and cardiovascular response, rather than study individuals on the basis of their reactivity to cardiovascular variables in isolation (e.g., Berntson et al., 1994). This strategy promises to provide more useful information on neural control of cardiovascular response during both rest and stress.

One of the fundamental assumptions of the importance of stress-related cardiovascular reactivity and cardiovascular disease is that reactivity exhibited by individuals shows consistency over time (Allen et al., 1987). This has traditionally been referred to as individual response stereotypy. Most theories of the manner in which reactivity can affect health outcomes assume that repeated exaggerated cardiovascular responses to stress may trigger maladaptive physiological processes. This implies a consistency of response when confronted by similar challenges at different points in time. Thus, studies have examined the temporal stability of cardiovascular response to laboratory or "real-life" challenges (e.g., Allen et al., 1987; Manuck & Garland, 1980). Although results have varied, most studies have found good consistency across time periods for measures such as heart rate, systolic blood pressure, and impedance cardiography-derived variables.

The issue of selection of an appropriate task to elicit cardiovascular reactivity has special relevance when considering the role of reactivity as a potential mediator between SES and health. As mentioned earlier, individuals living in low SES environments generally are exposed to more day-to-day stress than high SES individuals. Interestingly, one could speculate that greater chronic stress exposure could have either an accentuating or attenuating influence on acute stress exposure in cardiovascular reactivity paradigms. In the first instance, chronic exposure to stress would be conceptualized as already taxing a person's ability to cope with new, acute challenges. Individuals experiencing high levels of background chronic stress would show exaggerated acute stress responses (greater cardiovascular reactivity in this case) as compared to individuals exposed to minimal chronic stress. On the other hand, one could also envision that response to chronic stress might have a dampening effect on acute stress responses. This could be due to individuals having the time and opportunity to learn adaptations to stress (Matthews, Gump, Block, & Allen, 1997). A recent review of studies addressing the effects of background stress on acute reactivity and recovery from stress in a total of 19 studies indicated equivocal results, although heightened acute reactivity was found in a slight majority of the studies (Gump & Matthews, 1999). Among the many problems with the interpretations of these studies is the accurate measurement of background stress. Individuals within each study also show a wide range of individual differences in their acute responses, regardless of background stress. Clearly this is an unresolved issue that will require much additional study.

Finally, the "ecological validity" of measures of lab-based reactivity has been questioned. That is, some have argued that reactivity observed in sometimes contrived laboratory situations might not generalize to the "real world" and to the types of situations to which a person may be exposed in everyday life. This is especially important as it relates to differences in SES. Many of the commonly used laboratory tasks such as mental arithmetic or other problem-solving tasks may be differentially challenging to research participants who vary in intelligence and/or academic achievement. A person who is moderately challenged by the task may show more reactivity than one who is only minimally challenged. On the other hand, a person who finds the task to be exceedingly difficult may disengage from the task and show very little reactivity. Individuals from low SES environments may show more task disengagement because of a lack of adequate academic preparation, or they could become more easily frustrated because of the background chronic stress to which they are exposed. It is important to develop these tasks with built-in adjustments for task delivery so that the difficulty of the task will be roughly equivalent for all individuals. Tasks that require the individual to talk about unpleasant or stressful events in their lives can also vary considerably depending on SES. A high SES individual may discuss a situation concerning a rather benign disagreement at home or at school, whereas an individual living in a high crime area may discuss a shooting outside of his/her home. The point is that the researcher needs to consider whether the chosen task(s) to elicit acute reactivity may be differentially interpreted depending on SES status and differences in chronic stress.

Even if steps are taken to choose or modify tasks so as to minimize potential SES differences, there is still the issue of how well the reactivity seen during laboratory stressors index the reactivity exhibited by individuals in real-life interactions. Accordingly, a number of studies have compared laboratory-based reactivity with ambulatory responses, most often ambulatory blood pressure. The ambulatory monitors used in these studies are devices that usually measure both blood pressure and heart rate, but are small enough to be worn unobtrusively by the individual. These studies are important in trying to establish that laboratory-based reactivity is representative of the magnitude of response that individuals exhibit in everyday interactions.

Although there are conceptual difficulties in trying to find equivalent ambulatory periods with which to compare laboratory stress or resting periods (e.g., Pickering, 1993), many studies have found acceptable levels of correspondence between laboratory and ambulatory levels. For example, Linden and Con (1994) reported that an overall average of SBP reactivity during three laboratory challenges was a significant predictor of ambulatory blood pressure mean. Other studies have tried to specify more precisely the ambulatory periods that were likely to correspond to lab-based reactivity. Matthews et al. (1992) reported that the correspondence between ambulatory and lab BP values was strongest during the ambulatory periods of perceived stress. Thus, their conclusion was that ambulatory and lab-based BP responses were related, but one needed to take into account that the relationship is strengthened when appropriate ambulatory periods (such as times when the person is experiencing stress) are chosen. Steptoe et al. (2000) echoed these findings by reporting that ambulatory/lab associations were more consistent when the level of perceived stress and physical activity in the lab and field situations were more congruent. These studies point out that investigation in this area must go beyond merely correlating lab measures with overall ambulatory responses. To address whether lab-based reactivity can be generalized to the "real world," it is prudent to pick ambulatory periods that are similar in perceived stress to that experienced during the laboratory challenges.

What evidence is available to help one understand the potential relationship between cardiovascular reactivity and SES? To date, there have not been a large number of studies that have explored this issue, although a few informative studies are available. Lynch, Everson, Kaplan, Salonen and Salonen (1998) examined whether low SES and heightened cardiovascular reactivity had interactive effects on the progression of carotid atherosclerosis in men enrolled in the Kuopio, Finland study. In this study, cardiovascular reactivity was defined as the increase in SBP response in anticipation of a maximal exercise stress test. Results indicated that the greatest progression of atherosclerosis occurred in men who had both heightened reactivity and low SES. Although this study did not examine directly the relationship of SES and reactivity, the results with atherosclerosis risk suggest a natural clustering of SES and reactivity in determining a negative health outcome, rather than being independent factors. It is also of interest that an interaction was found; that is, the greatest progression of atherosclerosis was in a group that was not only low SES, but who were also more highly reactive. This suggests a moderating influence of reactivity on the relationship between SES and health outcomes.

A recent study by Gump et al. (1999) used structural equation modeling to examine the relationships among SES and cardiovascular reactivity in Black and White children. SES was defined in two ways: family SES was measured using the Four Factor Index of Social Status as devised by Hollingshead, and neighborhood SES was determined using information from census tract data such as educational attainment, percent of single mothers, and population density. The models relating SES and reactivity were different for Blacks and Whites. For Blacks, both neighborhood and family SES were negatively related to reactivity (higher SES associated with lower reactivity), with the relationships being mediated by hostility as measured by the Cook-Medley Ho scale. For Whites, family SES was negatively related to reactivity, although neighborhood SES was not. Interestingly, the family SES/reactivity relationship was not mediated via hostility. The reader is referred to Gump et al. for a detailed discussion of these intriguing findings. Although this study does not relate either SES or reactivity to a health outcome, the study does suggest that the relationship of SES and reactivity may also be modulated by other influences such as ethnicity or hostility.

The finding of increased reactivity being related to lower SES has not been found in all studies. Data from the Whitehall II study indicated that SBP increase during a mental stress task was associated with higher occupational grade (Carroll et al., 1997). Gump et al. (1999) have speculated that this finding in the Whitehall II study may have been due to the use of the Raven’s Progressive Matrices, a nonverbal intelligence test, as the mental stress. They suggest that this may have produced more effort and challenge in the high occupational group, and disengagement in the lower occupational group. The need to make sure that the laboratory challenges are as equivalent as possible for individuals from different SES levels was discussed in the last section.

Another line of research may indirectly point to a possible relationship between SES and reactivity. This is the study of race differences between Blacks and Whites with regard to cardiovascular reactivity. Studies in this area have usually either explicitly or implicitly assumed that any racial differences in reactivity were due to genetic differences, and in fact some differences in the baseline levels of heart rate and blood pressure have been found between Black and White infants (Schachter et al., 1974). Yet, it has been persuasively argued that social environment is a much stronger factor for racial differences than genetics. That is, some have suggested that race may be more accurately seen as a proxy for differences in SES between Blacks and Whites (Anderson et al., 1992). Viewed in this manner, racial differences in reactivity may shed light on SES and reactivity. To date, a number of studies have found greater vascular reactivity responses in Blacks than Whites (e.g., Treiber et al., 1990). There is evidence that Blacks may have more alpha-adrenergic responses to stress than Whites, with Blacks also exhibiting a blunted beta-adrenergic response. These stronger vascular responses are consistent with observations concerning the natural history of essential hypertension and the fact that Blacks have a higher incidence of hypertension and coronary heart disease than age-matched White counterparts. It is also interesting that a study by Allen and Matthews (1997) examined the effects of race on cardiovascular reactivity in a sample of children and adolescents in which the authors attempted to match Black and White participants on SES. Although the matching was not completely successful in equating SES in the groups, SES differences were less than in most reactivity studies examining race differences in young people. Interesting, no race differences in vasoconstrictive responses were found in this study. This is consistent with the notion that at least some of the racial differences in vasoconstrictive responses reported in other studies may be related to lower SES in the Black samples. One might also speculate that reactivity differences are not as easily found in samples of children and adolescents as in adult samples due to the longer exposure to the stress of lower SES lifestyles and neighborhoods in adults. Obviously, much additional research is needed to further illuminate these issues.

Although the research question of the importance of exaggerated cardiovascular responses to stress for deleterious cardiovascular health outcomes has been asked for many years, the direct evidence for this relationship is still sparse. One of the obvious reasons for this is that longitudinal studies are needed to effectively address these questions. Individuals with already established cardiovascular disease cannot be used as the disease process itself will alter the cardiovascular responses to stress. The area that has been most commonly addressed is the degree to which exaggerated cardiovascular reactivity is a risk factor for hypertension (an excellent review is Lovallo and Wilson, (1992)).

Most of the longitudinal studies to date have used reactivity to dynamic exercise or the cold pressor test as predictors for hypertension. Studies such as Jackson et al. (1983) and Wilson and Meyer (1981) have reported that future hypertension in previously normotensive adults was predicted by blood pressure responses to dynamic exercise. The cardiovascular responses of individuals during the cold pressor test (immersion of hand or foot in ice water) have been examined longitudinally in a few studies. For example, Menkes et al. (1989) report the findings on 910 White, male medical students who had blood pressure and pulse rate measured before and during a cold pressor test (tested between 1948-1964). A significant association was found between maximal change in SBP during the cold pressor test and subsequent development of hypertension after many years. This relationship persisted even after controlling for such factors as cigarette smoking, initial resting SBP, and family history of hypertension. Data from the Bogalusa Heart Study on children (Parker et al., 1987) indicate that peak cardiovascular reactivity during three physical challenges (orthostatic challenge, handgrip exercise, and the cold pressor) predicted SBP and DBP resting levels four years later. It should be noted that some studies have not found this relationship. For example, Carroll et al. (1996) report that DBP reaction to the cold pressor test in a group of 1039 men explained only a very small portion of the variance in follow-up DBP after 5 years (SBP had no explanatory power). However, the men in the Carroll et al. study averaged 56.6 years of age, whereas the participants in the Menkes et al. study were young medical students. As most researchers posit that excessive reactivity may predict neurogenic hypertension that may have a relatively early onset, the young sample in the Menkes study may be a more appropriate sample.

The various hypotheses concerning the potential role of psychological stress as a factor in the etiology of cardiovascular disease have generally emphasized the deleterious effects of excessive sympathetic nervous system activation on the cardiovascular system, although parasympathetic withdrawal has also been considered. One stimulus for this line of inquiry has been animal studies reporting sustained elevations in blood pressure in certain genetic strains of rats who were subjected to stressful conflict avoidance situations (e.g., Lawler et al., 1980), as well as elevated blood pressure in mice who were housed in overcrowded conditions (e.g., Henry et al., 1975). Therefore, a few longitudinal studies have examined the predictive power of responses to psychologically challenging situations on later blood pressure status.

Borghi et al. (1986) reported that the magnitude of the DBP responses during a mental arithmetic challenge significantly predicted the increase in blood pressure after 5 years in young borderline hypertensive individuals. Everson et al. (1996), in a study of middle-aged men in Kuopio, Finland, investigated whether the rise in BP in anticipation of a bicycle ergometer stress test was related to subsequent longitudinal increases in resting BP. Results indicated that men exhibiting either an anticipatory SBP response greater than or equal to 30 mm Hg or a DBP response greater than or equal to 15 mm Hg had nearly four times the risk of developing hypertension after a 4 year period. This relationship was maintained even after controlling for traditional risk factors for hypertension. Light et al. (1992) reported that SBP and heart rate responses to a challenging reaction time task were significant predictors of blood pressure status after a 10-15 year period. The participants in this study were college students at the initial testing, and all initially were normotensive males. In analyzing data from the CARDIA study on young normotensive men and women, Markovitz et al. (1998) report that increased SBP reactivity during a challenging video game was associated with increased SBP after 5 years, independent of resting SBP. Interestingly, this relationship was found to hold for men but not women. This study did not find a predictive relationship for reactivity during the cold pressor or mirror tracing task and subsequent BP levels.

Matthews et al. (1993) examined the prognostic value of cardiovascular reactivity for follow-up blood pressure in male and female children. The measure of reactivity included a composite standardized reactivity score during mirror tracing, mental arithmetic and isometric handgrip. Among boys only, larger blood pressure reactivity scores were associated with greater blood pressure levels after 6 ½ years. Similar findings using a video game as the psychological stressor were found by Murphy et al. (1992). Thus, there are a number of studies that have reported that some aspect of cardiovascular reactivity does predict later levels of blood pressure, although the relationship may be stronger for males than females.

Although most studies in this area have examined the relationship of cardiovascular reactivity to physical or psychological challenges and future increases in BP or development of hypertension, a few studies have investigated whether reactivity is related to cardiovascular disease progression in individuals who already have documented disease. For example, Manuck et al. (1992) report the results of a pilot study on 14 individuals who had already experienced a myocardial infarction. Five of these individuals subsequently suffered either a reinfarction or stroke. These five individuals had previously shown significantly larger increases in SBP and DBP during a frustrating Stroop Color-Word Interference task than the remaining individuals who had not experienced a second clinical event. In a related study, Barnett et al. (1997) report that the amount of carotid artery plaque development over a 2 year period in a group of 136 untreated patients was significantly related to SBP reactivity during the Stroop test, along with a number of traditional risk factors. These studies suggest that cardiovascular reactivity to psychological stress can influence the development of atherosclerosis in susceptible patients.

A number of epidemiological studies have found that lower SES is associated with increased risk for a negative cardiovascular health outcome. To what extent can reactivity protocols help one to understand the SES-health gradient? Does reactivity serve a moderating role whereby individuals who are both highly reactive and experience the burden of a chronic stressful environment are at greater risk for deleterious health outcomes? At least one study from the Kuopio, Finland studies points to this moderating role of reactivity. There is also the possibility that chronic exposure to stress by low SES individuals leads to a developed pattern of responding to the environment with anticipated threat or challenge. The concurrent heightened physiological reactivity during these behavioral patterns may, over time, result in negative health outcomes. This is consistent with findings from studies like Gump et al. (1999) which finds that heightened vasoconstrictive responses are associated with lower SES. But it is also the case that ethnicity and/or characteristics like hostility may moderate these relationships. Thus, reactivity may link SES and health outcomes, although the precise role of reactivity will require much more study. This role may be in conjunction with, rather than in lieu of, other potential mediators of the SES/health connection such as diet, availability of medical care, adherence to treatment regimens, etc.

There are a number of factors that make it difficult to test the role of reactivity in linking SES and health outcomes. First, the definition of reactivity has varied from study to study. Whether to use heart rate, blood pressure, cardiac performance variables, vascular resistance, or a combination of multiple measures into cardiovascular patterns, has varied from study to study. Other factors are whether to use laboratory-based or ambulatory-based challenges. How to measure change from a baseline period to a task or challenge period has also been debated. One thing does seem clear. For the field of reactivity research to progress, researchers, whether in psychology, behavioral medicine, health psychology or others, examining reactivity relationships with SES and/or health outcomes must understand basic cardiovascular physiology rather than conceive of cardiovascular variables such as heart rate and blood pressure as ends in themselves. It will not be enough to simply report an increase in, say, blood pressure; rather, one must try to understand the adjustments made by the entire cardiovascular system and the autonomic underpinnings of those adjustments. We must, as the late Paul Obrist was oft to say, become "better biologists" (Brener, 1988).

Finally, the total reliance on large-n studies to elucidate the patterns of cardiovascular adjustments to challenge is being challenged on a number of fronts. The traditional way of comparing large groups of individuals to discover characteristic cardiovascular patterns of response results in data that have been "homogenized" across a large number of individuals. These mean responses of groups give one a stable, average characterization of response patterns, but much of the richness of the data from individuals is lost. A growing number of researchers (e.g., Friedman & Thayer, 1998) are calling for a more "idiographic" approach to understanding cardiovascular dynamics during stress. The strategy here is to study a relatively small number of individuals, but to do extensive evaluation of these individuals under a number of challenging and baseline conditions. This "case study" approach, as opposed to the more "epidemiological" approach of the large-n studies, may more accurately assess the pattern of cardiovascular adjustments exhibited by individuals. This is not to say that the traditional large-n studies should be replaced by the idiographic studies; the development of statistics for the small-n studies has not progressed as rapidly as the traditional designs, and most funding sources such as the National Institutes of Health are not accustomed to funding studies where power determination is unclear. Rather, the small-n studies would complement the findings from the large-n studies. This is an important conceptual area to be addressed when looking at the future of cardiovascular reactivity research.

Selected Bibliography

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Allen, M.T., & Matthews, K.A. (1997). Hemodynamic responses to laboratory stressors in children and adolescents: The influences of age, race, and gender. Psychophysiology, 34, 329-339.

Allen, M.T., Sherwood, A., Obrist, P.A., Crowell, M.D., & Grange, L.A. (1987). Stability of cardiovascular reactivity to laboratory stressors: A 2 ½ year follow-up. Journal of Psychosomatic Research, 31, 639-645.

Anderson, N.B., McNeilly, M., & Myers, H.F. (1992). Toward understanding race difference in autonomic reactivity: A proposed contextual model. In Individual differences in cardiovascular response to stress. J.R. Turner, A. Sherwood, and K.C. Light (Eds.). Plenum: New York, 125-145.

Barnett, P.A., Spence, J.D., Manuck, S.B., & Jennings, J.R. (1997). Psychological stress and the progression of carotid artery disease. Journal of Hypertension, 15, 49-55.

Berntson, G.G., Cacioppo, J.T., Binkley, P.F., Uchino, B.N., Quigley, K.S., & Fieldstone, A. (1994). Autonomic cardiac control. III. Psychological stress and cardiac response in autonomic space as revealed by pharmacological blockades. Psychophysiology, 31, 599-608.

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Carroll, D., Davey-Smith, G., Sheffield, D., Shipley, M.J., & Marmot, M.G. (1997). The relationship between socioeconomic status, hostility, and blood pressure reactions to mental stress in men: Data from the Whitehall II study. Health Psychology, 16, 131-136.

Carroll, D., Davey-Smith, G., Sheffield, D., Willemsen, G., Sweetnam, P.M., Gallacher, J.E., & Elwood, P.C. (1996). Blood pressure reactions to the cold pressor test and the prediction of future blood pressure status: Data from the Caerphilly study. Journal of Human Hypertension, 10, 777-780.

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Everson, S.A., Kaplan, G.A., Goldberg, D.E., & Salonen, J.T. (1996). Anticipatory blood pressure response to exercise predicts future high blood pressure in middle-aged men. Hypertension, 27, 1059-1064.

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Lynch, J.W., Everson, S.A., Kaplan, G.A., Salonen, R, & Salonen, J.T. (1998). Does low socioeconomic status potentiate the effects of heightened cardiovascular responses to stress on the progression of carotid atherosclerosis? American Journal of Public Health, 88, 389-394.

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Matthews, K.A., Woodall, K.L., & Allen, M.T. (1993). Cardiovascular reactivity to stress predicts future blood pressure status. Hypertension, 22, 479-485.

Markovitz, J.H., Raczynski, J.M., Wallace, D., Chettur, V., & Chesney, M.A. (1998). Cardiovascular reactivity to video game predicts subsequent blood pressure increases in young men: The CARDIA study. Psychosomatic Medicine, 60, 186-191.

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Menkes, M.S., Matthews, K.A., Krantz, D.S., Lundberg, U., Mead, L.A., Qaqish, B., Liang, K.-Y., Thomas, C.B., & Pearson, T.A. (1989). Cardiovascular reactivity to the cold pressor test as a predictor of hypertension. Hypertension, 14, 524-530.

Parker, F.C., Croft, J.B., Cresanta, J.L., Freedman, D.S., Burke, G.L., Webber, L.S., & Berenson, G.S. (1987). The association between cardiovascular response tasks and future blood pressure levels in children: Bogalusa Heart Study. American Heart Journal, 113, 1174-1179.

Pickering, T.G. (1993). Applications of ambulatory blood pressure monitoring in behavioral medicine. Annals of Behavioral Medicine, 15, 26-32.

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