Although homeostasis is a common characteristic of the underlying physiology of humans and most other life forms, our regulatory systems possess the adaptive capacity to mount relatively dramatic temporary changes to respond to and even anticipate challenges. For the cardiovascular system, some challenges are as simple and routine as changing from supine to standing posture. Others involve dealing with complex interpersonal interactions based on prior learning and experience, like job interviews or driving a car in heavy traffic. The regulatory systems that allow transitory increases in blood pressure, heart rate, cardiac output, and/or vasoconstriction include efferent activity via sympathetic and parasympathetic nerves to the heart and blood vessels; adrenocortical and adrenomedullary hormones such as epinephrine, norepinephrine, and Cortisol; neuropeptides such as oxytocin, vasopressin, and atrial natriuretic peptide; and other substances with endocrine activity. The hypothalamus plays a major role in the integration of cardiovascular responses and thus is always part of the initiation, maintenance, and post task recovery of cardiovascular responses to behavioral events.
Historically, the best-recognized pattern of cardiovascular responses has been labeled the defense reaction, an increase in heart rate and blood pressure and a decrease in vasoconstriction seen in cats during hypothalamic stimulation that also engaged motor responses mimicking those occurring when the animal was faced with a predator. Also described as the fight-or-flight response, the hemodynamic adjustments were adaptively designed to mobilize the cardiovascular system to provide extra oxygenated blood flow to working muscles before and during vigorous activity. In modern industrialized societies, however, the remnants of this response pattern (minus much of the dilation of blood vessels) are frequently evoked during cognitive and emotional stressors where physical activity does not increase. Then the mobilization increases cardiac work and stresses the vasculature with no apparent benefit.
The primary interest in human research on cardiovascular reactivity is actually on the study of individual differences. Who is a high reactor to this challenge and who is a low reactor? Can we use the magnitude of reactivity or change in physiological response to reveal an underlying response that is excessively great or small, and therefore indicates dysregulation in a key physiological system? Can we show that someone who is a high reactor to one challenge will be a high reactor to others, and will high or low responses to laboratory stressors reflect the relative responses to natural life demands?
The classic reactivity hypothesis in its most general form posits that individuals who are high reactors to behavioral challenges or stressors will over time be more likely to develop elevated blood pressure and hypertensive heart disease (characterized by left ventricular remodeling and hypertrophy) and/or coronary heart disease (characterized by stenosis in coronary vessels, which can lead to myocardial infarction). High stress response may be simply a marker of increased cardiovascular risk, or it may play a more direct role. In the latter case, it is suggested that transitory episodes of elevated adrenergic and cardiovascular activity, if evoked on a frequent basis by stressors in an individual’s environment at home or work, may eventually induce secondary changes leading to resetting of homeostatic mechanisms to a higher level of blood pressure (BP) maintained even in the resting state, and to structural changes in the heart and vessels.
The reactivity hypothesis has generated considerable research and much debate since the 1970s. High heart rate, blood pressure, cardiac output, and vascular resistance responses to stressors have been shown to be relatively stable characteristics of certain individual across challenges and over time intervals from a few months to as long as 10 years. Several longitudinal studies have confirmed the expected association between high cardiovascular response to stressors and higher incidence of hypertension, but others have found this relationship to be modest or absent after partialing out higher resting BP, which is associated with both high stress response and later hypertension. In two recent prospective studies, high pressor response to active coping tasks predicted increased BP after 5 and 6.5 years of follow-up in men but not women, and showed stronger relationships in persons of lower than of higher socioeconomic status (SES). This may be related to the fact that women have a low incidence of hypertension prior to the age of menopause, perhaps due to protective effects of reproductive hormones, and to the likelihood that lower-SES persons are exposed to greater economic and social stress.
Updated variations of the reactivity hypothesis differ from the original in several respects, but are likely to yield stronger predictive relationships to cardiovascular disease outcomes. First, using BP reactivity scores in a simple linear regression model to predict subsequent BP or hypertension seems much less powerful than comparing individuals in the highest quartile (top 25%) versus the lower three quartiles of reactivity. That is, there appears to be a threshold effect rather than a continuous increment of risk. Second, one recent 10-year follow-up study demonstrated that high stress responses were much more predictive of later hypertension among those with genetic susceptibility, defined as one or more hypertensive parents, and risk was further enhanced in those reporting greater daily life stress exposure. Thus, it is recommended that future tests of the reactivity hypothesis should be specifically designed to examine interactions between extreme versus lesser cardiovascular responsivity and family history of hypertension or other indexes of enhanced genetic or environmental susceptibility.
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