The influence of behaviors on the development and progression of coronary heart disease (CHD) is thought to involve both psychosocial and physiological processes. For example, high blood pressure, high serum cholesterol, and cigarette smoking, considered to be risk factors for CHD, are each affected by behavior. One avenue of research has attempted to determine the direct effects of coronary-prone behaviors on physiological responses to environmental stimuli. It has been hypothesized that the link between coronary-prone behaviors and CHD involves excessive or prolonged hyperactivation of the sympathetic nervous system (SNS; Krantz & Manuck, 1984). It is believed that pronounced and recurrent activation of the SNS by particular behavioral stimuli can precipitate endothelial injury, and thus promote atherosclerotic plaque build-up (Ross & Glomset, 1973). Animal studies (Manuck, Muldoon, Kaplan, Adams, & Polefrone, 1989) have indicated that behaviorally induced cardiovascular (CV) hyperactivity is significantly positively associated with degree of intimal damage and severity of coronary artery disease (CAD). Although there is a paucity of evidence suggesting a direct link between behaviorally induced CV changes and CHD in man, results from two longitudinal studies have indicated that the cold pressor test (Keys, Taylor, Blackburn, Brozck, Anderson, & Somonson, 1971) and changes in posture (Sparrow, Tifft, Rosner, & Weiss, 1984) evoke diastolic blood pressure (DBP) responses that are positively associated with risk of CHD. Consistent with the notion of hyperresponsitivity as a contributing factor for CHD, some studies (Corse, Manuck, Cantwell, Giordani, & Matthews, 1982; Dembroski, MacDougall, & Lushene, 1979) have shown that cardiac patients, relative to noncoronary 176patient controls, respond with greater physiological increases to behavioral stressors.