Abstract
To determine the contributions of the sympathetic and parasympathetic systems to cardiovascular stress reactivity, a meta-analysis was undertaken. The original literature search yielded 26,761 manuscripts; 203 were of sufficient quality and measured indices of sympathetic and/or parasympathetic activity resulting in an overall sample of 9,691 participants. A range of psychological stressors reliably perturbed cardiovascular function as indexed by blood pressure and heart rate (p’s < .001). Significant aggregate effects revealed a pattern of autonomic reactivity characterized by increased plasma epinephrine (69 studies, p < .001) and norepinephrine (72 studies, p < .001), decreased pre-ejection period (75 studies, p < .001) and vagal withdrawal (120 studies, p < .001). Subgroup analyses indicated variations in effect size according to stress task, gender, and age. Pharmacological manipulation of cardiovascular reactivity (29 studies) by alpha- and beta-adrenergic blockade showed that the former failed to influence reactivity (p = .474) while the latter significantly reduced heart rate and systolic blood pressure effect sizes (p < .001). Atropine failed to attenuate stress responses in one study. Overall, results indicated that cardiovascular reactivity to acute psychological stress is primarily driven by beta-adrenergic activation and vagal withdrawal.
Original language | English |
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Title of host publication | 72nd Annual Scientific Meeting |
Subtitle of host publication | Stretching the Boundaries: From Mechanisms of Disease to Models of Health |
Publisher | American Psychosomatic Society |
Pages | 49 |
Number of pages | 1 |
Publication status | Published - 13 Mar 2014 |
Event | American Psychosomatic Society - San Francisco, United States Duration: 12 Mar 2014 → 15 Mar 2014 |
Conference
Conference | American Psychosomatic Society |
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Country/Territory | United States |
City | San Francisco |
Period | 12/03/14 → 15/03/14 |