From evidence presented in Chapter 5, it appears that the intensity, duration, or patterning of the acute physiological response to stress is the most likely candidate for mediating the stress-hypertension relation. Certainly, among all other aspects of the acute stress response, physiological reactions are the most plausible mediators. If acute cognitive, behavioral, or affective responses were shown to mediate the stress-hypertension relation, we would still be left with quite a challenge of establishing how a specific thought, behavior, or emotion could possibly lead to vascular hypertrophy or baroreceptor insensi-tivity associated with the condition of prolonged essential hypertension. At least, with regard to acute physiological stress responses, plausible explanations exist regarding how hyper-responsive circulatory systems evolve into chronic problems in blood pressure regulation. For example, the description of the hyperkinetic borderline hypertensive patients established by Julius and Esler (1975) and the evolution of problems in blood pressure regulation from cardiac-mediation to subsequent vascular involvement (Laragh, 1983; Lund-Johansen, 1991) are both consistent with a focus on the sympathetic nervous system in the etiology of hypertension, at least for a subgroup of hypertensive patients.
Although acute physiological responses to stress are likely candidates for mediating the stress-hypertension link, it is obvious that individual differences in physiological responses to stress exist and need to be considered in any model of hypertension. For example, exposure to stressful life events, jobs, or cultures leads to acute elevations in blood pressure among some individuals, whereas other individuals exposed to identical stressful life events, jobs, or cultures maintain normal blood pressure responses. A wide array of individual difference variables has been examined that have been hypothesized to influence the magnitude and pattern of physiological stress responding, including constitutional parameters (like gender or ethnicity) and psychosocial characteristics (like coping skills, personality, and social support). These variables cannot technically be considered candidates for mediating the stress-hypertension relation in the model presented in Figure 4.1, because they are not elicited by stress; rather, they represent independent factors that are present regardless of whether an individual is exposed to stressful stimuli or not. For example, stress does not lead to altered constitutional characteristics like a change in gender or ethnicity. Likewise, personality and related trait-like phenomena are not typically influenced by the sudden onset of an environmental stressor. Nevertheless, these variables have been hypothesized to play a role in the etiology of essential hypertension, perhaps through their association with the acute response to environmental stress.
This chapter will examine evidence for potential individual difference variables pertaining to constitutional and lifestyle factors that influence both the stress-hypertension relation and the stress-cardiovascular reactivity relation. These individual difference parameters may also predict risk for hypertension independently. However, in order for them to be considered individual difference factors associated with the stress-hypertension relation and facilitate our understanding of how stress might lead to hypertension, they must also interact with exposure to stress to influence the magnitude and patterning of the acute cardiovascular stress response. For example, it is well known that obesity is an individual difference variable that is directly associated with increased risk for essential hypertension. The increased risk for hypertension associated with obesity is evident regardless of the stress-fulness of one's life. In this respect, obesity represents a direct influence upon risk for hypertension. If obese individuals with high levels of stress exhibited a greater incidence of essential hypertension than non-stressed obese individuals, obesity might also be said to influence the stress-hypertension relation in addition to its direct effect on risk for hypertension. Additionally, if obese persons were shown to exhibit exaggerated cardiovascular responses to stress in contrast to normal-weight controls, evidence for obesity as affecting the stress-cardiovascular reactivity relation would also be demonstrated. Both sources of evidence are considered for the potential constitutional and lifestyle factors in this chapter. Potential psychological and social factors involved in the stress-hypertension relation are described in Chapter 7.
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