Some Working Hypotheses on the Significance of Behaviorally Evoked Cardiovascular Reactivity to Pathophysiology

A guiding hypothesis inherent in research on the role of behavioral influences in the etiology of cardiovascular pathophysiology is that repeated occurrences of environmentally induced myocardial, vascular, and blood pressure (BP) reactivity is the means by which life’s events are translated into the disease process (Folkow 1982). While this assumption appears to have a certain face validity, there is evidence to indicate that reactivity per se does not have invariable pathophysiological consequences, since there are circumstances where reactivity serves a necessary adaptive function. For example, pressor responses facilitate tissue perfusion when one exercises (Obrist 1981) or changes state from sleep to awake (Floras et al. 1978). On other occasions, reactivity may reflect nothing more than a momentary disruption in the efficiency with which the individual adjusts cardiovascularly to the ever-changing events in the interaction of the organism and its environment (Obrist et al. 1970; Obrist 1984). The most definitive evidence implicating this interaction, and hence reactivity, in the development of cardiovascular disease, is from animal models (Lawler et al. 1981; Anderson et al. 1983; Kaplan et al. 1983; Manuck et al. 1983). But caution must be exerted in generalizing from such data, since we are not certain how much one can liken these models to the human condition. This paper is intended first to briefly overview some of the evidence which places some reservations on this hypothesis, and secondly to propose some specific hypotheses that attempt to provide a perspective of how we might better decipher when reactivity has the pathophysiological consequences we seek to ascertain. This discussion is most relevant to the hypertensive process but is also applicable to coronary heart disease, to the extent that hypertension is instrumental in the development of atherosclerosis.