ReviewAn historical context for behavioral models of hypertension
Section snippets
Overview
Stress and other behavioral factors such as social support have been linked to a broad range of cardiovascular disease outcomes, including coronary heart disease 1, 2 and hypertension 1, 3. The mechanisms, or pathways, through which these influences operate, however, remain controversial. We will discuss the evolution and characteristics of four different psychophysiological reactivity models that focus on the relationship between stress and the development of hypertension. In the earliest
Reactivity as a marker for hypertension risk (model 1)
In 1932, Hines and Brown [6] published the first account of cardiovascular reactivity testing. The motivation for their study was to develop a simple procedure, applicable in the doctor's office, for identifying future cases of hypertension. This rationale was clearly laid out in a study by Ayman and Goldshine, published in 1938 [8]. They noted:
Many young people are certain to develop essential hypertension some day. If it were possible to apply a standard stimulus to such people, it might be
Reactivity as a trait-based contributing cause to the development of hypertension (model 2)
In the past few decades, the causal model of reactivity has been adopted by most researchers in this area and, consequently, reactivity has been embraced as the most likely mechanism through which stress adversely affects cardiovascular health. This revised formulation—that cardiovascular reactivity plays a causal role in the development of hypertension—has an important implication concerning the notion of exposure; that is, for reactivity to play a casual role in the mediation of the
Reactivity as a situation-based contributing cause in the development of hypertension (model 3)
Like model 2, model 3 hypothesizes that reactivity plays a causal role in the development of hypertension. However, rather than focusing on trait dimensions, which places the emphasis on characteristic responses of the individual, model 3 focuses on dimensions of the situation that tend to elicit blood pressure and heart rate reactivity. Thus, model 3 posits that individuals who are exposed to stressful situations, and therefore exhibit exaggerated reactivity with some degree of frequency, are
Reactivity as a person-by-situation cause of hypertension (model 4)
It is likely that many factors—person and situation—contribute, perhaps interactively, to the disease process. Some individuals are thought to be predisposed to display larger blood pressure and heart rate reactivity, operating through one or another personality dimension, such as anger expression or hostility. Such exaggerated reactions may only occur, however, when the person is exposed to circumstances that are relevant to this trait (e.g., in a frustrating situation). Thus, some researchers
Reactivity model—as it appears today
The 70 years of cardiovascular reactivity literature reveal several controversies, and many of these remain unresolved. There is little consensus, for example, on the specific physiological mechanisms involved in the development of hypertension. In addition, we and others have suggested that reactivity—the response that occurs while the stressor is present—may not be the most important aspect of the stress–hypertension relation. Recovery of prestress resting levels, we suggest, may be an
Summary and conclusions
Hines and Brown began, in 1932, with a simple and straightforward question: Can we devise a simple test that will predict future hypertension? [5]. Such a test still does not exist, and that reveals something about the difficulties encountered in such an endeavor. Although some studies show a relationship between reactivity and blood pressure level, or hypertension status, the observed relationships are not strong enough to allow us to make predictions on a case-by-case basis. However, future
Acknowledgements
Funding for this study was provided by National Institutes of Health Grant P01 HL 47540.
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