A widely held hypothesis is that cardiovascular hyperreactivity is a risk factor for the development of essential hypertension. Cardiovascular hyperreactivity is defined as an exaggerated cardiovascular response to a stressor. In the past few decades, reactivity has been regarded as the most likely mechanism through which stress contributes to the long-term development of hypertension, or more precisely the initiation of its development. However, despite years of investigation, the precise role played by cardiovascular hyperreactivity in the development of hypertension remains largely unknown.
Several biological mechanisms that may mediate the relationship between reactivity and hypertension have been proposed. Indeed, these mechanisms may provide links between reactivity and hypertension. The reactivity hypothesis draws on the response of the sympathetic nervous system to stressful environmental stimuli. Studies of the response of the sympathetic nervous system to stress involve several limitations. First, the effect of any given stressful stimuli has limited reproducibility. An individual can respond to one stressor with profound cardiovascular responses and respond to other stressors without cardiovascular arousal. Second, laboratory stressors have limited external validity. Some suggest that the blood pressure response or reactivity to laboratory stressors does not predict ambulatory blood pressure during everyday life. Finally, it has been argued that the sympathetic nervous system is not important in the long-term regulation of arterial pressure. This argument is based on the observation that several conditions with marked sympathetic activation, such as heart failure, cirrhosis, and panic disorder, are not accompanied by increased arterial pressure.
This presentation will review the construct of reactivity and its measurement issues. A critical analysis of various hypothesized biological links between cardiovascular hyperreactivity and hypertension will be addressed. This presentation shall provide new insights into the role of cardiovascular hyperreactivity in the development of hypertension.
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