Psychophysiological reactivity: mechanisms and pathways to cardiovascular disease.

OBJECTIVE This article examines possible sources of heightened psychophysiological reactivity in relation to risk for hypertension and coronary artery disease. The idea that exaggerated reactions to psychological stress may predict greater risk for future disease has some support in the psychosomatic and behavioral medicine literature. However, the pathways by which exaggerated reactivity could arise in a given person and the implications of different sources of reactivity for potential disease relationships have received little attention. METHODS This topic is approached through a selective literature review and by means of a neurophysiologically based model of individual differences in physiological reactivity. Temperament characteristics, cognitive processes, neurophysiology, and peripheral physiology are used to indicate three levels that could contribute to exaggerated physiological reactivity. RESULTS At the top level in the model, activity of the frontal cortex and limbic system establish cognitive-emotional sources of activation that may underlie exaggerated physiological reactivity. In the absence of these influences, large responses may be more likely when exaggerated subcortical response tendencies are present via the hypothalamus or brain stem. Finally, peripheral alterations may account for larger reactions in persons who have otherwise normal emotional and hypothalamic and brainstem response tendencies. Cognitive-emotional and hypothalamic-brainstem sources of altered reactivity may cause or aggravate disease. In contrast, altered peripheral reactivity suggests that a pathophysiologic process may be present, serving as a marker for disease. CONCLUSIONS These three levels of analysis allow for organization of existing data in the area of cardiovascular reactivity and for planning future studies in a hypothesis-building framework.