Abstract
Recently, considerable debate has been sparked concerning the strength of published evidence supporting what has been called “the Reactivity Hypothesis.” This hypothesis, as most broadly defined, is that greater cardiovascular reactivity to behavioral stressors may play some role in the development of sustained arterial hypertension. Thus, when focusing on the wide individual differences in blood pressure, heart rate, cardiac output, or any other cardiovascular responses that are evoked by a stressor, it is postulated that the high reactors will have an increased risk of becoming hypertensive over time. Some researchers (Pickering & Gerin, 1990) do not find the current evidence supporting this hypothesis to be compelling, citing, among other things, the lack of many prospective investigations showing that high reactivity is a significant independent risk factor. Other authorities (Manuck, Kasprowicz, & Muldoon, 1990) prefer to see the glass half full rather than half empty, and they find the combination of a great deal of consistently supportive indirect evidence and positive results from the relatively few prospective studies to encourage further, better-designed tests of the Reactivity Hypothesis.
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Light, K.C., Sherwood, A., Turner, J.R. (1992). High Cardiovascular Reactivity to Stress. In: Turner, J.R., Sherwood, A., Light, K.C. (eds) Individual Differences in Cardiovascular Response to Stress. Perspectives on Individual Differences. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-0697-7_15
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DOI: https://doi.org/10.1007/978-1-4899-0697-7_15
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