Author: Quartana PJ, Burns JW.
Affiliation:
Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA. pquarta1@son.jhmi.edu
Conference/Journal: Br J Health Psychol.
Date published: 2010 Sep
Other:
Volume ID: 15 , Issue ID: Pt 3 , Pages: 511-28 , Word Count: 245
OBJECTIVE: The study of anger suppression and risk for cardiovascular disease has relied predominately on inspection of correlations between trait anger-in and cardiovascular risk factors and disease. This approach tells us little about whether inhibitory processes have anything to do with outcomes, and cannot speak to whether suppression of anger per se affects cardiovascular parameters. Drawing on the broader emotion regulation literature, we examined the effects of experimentally induced anger and general negative emotion in the context of expressive and experiential suppression on cardiovascular responses to initial and subsequent laboratory stressors.
DESIGN: Of all participants, 201 healthy participants were randomly assigned to one of six conditions formed by crossing emotion (anxiety, anger) and suppression (experiential, expressive, control) conditions.
METHODS: Participants completed a mental arithmetic task with anxiety or anger induction under their respective suppression manipulation instructions, and subsequently were exposed to a cold pressor task. Systolic blood pressure (SBP), diastolic blood pressure, and heart rate values were obtained for each experimental epoch.
RESULTS: More robust SBP responses to the initial stressor were evidenced for those in the expressive versus the control condition. In response to the subsequent stressor, those in the experiential suppression condition showed the most pronounced SBP responses, suggesting pronounced delayed effects of this type of suppression. Effects of suppression on SBP reactivity were indistinguishable across anxiety and anger conditions.
CONCLUSION: Effortful suppression of negative emotion has immediate and delayed consequences for stress-induced cardiovascular reactivity. Theoretical and clinical significance of these findings are discussed.