Cardiovascular reactivity: mechanisms and pathways to cardiovascular disease.

Researchers in physiology, psychology, and medicine have held the idea that risk for cardiovascular disease is increased by exaggerated responses to stress. Some epidemiological evidence supports this view and shows that exaggerated blood pressure responses to stress add to disease prediction beyond that provided by standard risk factors. Most studies of reactivity and disease risk have taken a correlational approach to the reactivity-disease relationship. This paper presents a model of central nervous system control over peripheral response systems that provides a way of designating three sources of exaggerated stress reactivity that may vary across individuals. The top level in the model consists of the limbic system and prefrontal cortex as interacting areas that form psychological stress responses. These frontal-limbic interactions are a means of translating experiential and affective processes into bodily responses. The middle level consists of hypothalamus and brainstem areas that translate descending influences into bodily outputs. Activation levels in these structures can lead to enhanced reactivity to many forms of challenge. The final level consists of the peripheral effectors that create the response itself; altered effector function can be a source of enhanced reactivity. Study designs that involve both psychological and physiological challenges and that take account of self-reports of affect and activation provide a basis for separating these sources of responsivity. This organization may provide useful insights into the sources of stress reactivity that characterize specific groups at risk and allow inferences as to the source of the disease pathophysiology.