A large body of research indicates stress-related mechanisms are involved in the development of hypertension (HTN). Exaggerated cardiovascular reactivity (CVR) to acute, laboratory-induced stress has been associated with later onset of HTN fairly consistently across studies. Early studies examining the role of CVR as an independent or "isolated" risk factor for HTN, however, have repeatedly shown CVR's limited predictive capability. In those studies, CVR has accounted for <10% of the variance over resting blood pressure. More recent findings have demonstrated that stress-related mechanisms of HTN development are likely to be multifactorial in nature, and involve interaction effects. Given the scientific progress in this area, it has become increasingly apparent that predictive models of stress-related HTN development must become more complex and multifaceted if they are to be clinically useful. Thus, person, situation, and environmental factors need to be considered simultaneously, as these factors are likely to have cumulative effects, resulting in a "composite" risk factor. Using the Allostatic Load model as a template, this paper presents a model for examining the relationships between stress and 24-hour ambulatory blood pressure over time among persons with pre-existing risk factors for HTN. Specifically, person factors (parental history of HTN, high normal blood pressure), person X situation factors (CVR to anger recall, perceived stress, psychological distress, race), and situation X environmental factors (socioeconomic status and individual + neighborhood social supports) are considered simultaneously. One purpose of this model is to further examine the role that social determinants (such as socioeconomic status and race) play in contributing to cardiovascular health disparities. While family history and health behaviors are known to contribute to the risk of higher blood pressure, a number of epidemiologic studies have demonstrated that social and economic factors are also strong determinants of HTN and cardiovascular disease prevalence, even when controlling for health behaviors (smoking, obesity, exercise) as potential confounders. Some evidence suggests that greater exposure to recurrent and/or chronic stress associated with material deprivation, lack of individual social supports, neighborhood cohesion, and discriminatory practices all contribute to the sympathetic activation that underlies CVR, and hence the development of HTN. The extent to which social or economic characteristics may be causal factors in HTN development, however, is likely to also depend on person factors such as genetic predisposition and cognitive or behavioral responses to stressors. This presentation provides a fresh perspective on the utility of multifactoral models that account for the effects of stress from the broader environment--particularly in persons predisposed to HTN. The potential for such models to yield findings applicable to clinical practice will be discussed.
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