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Heart Rate, Neuroendocrine, and Immunological Reactivity in Response to an Acute Laboratory Stressor

From the Center for Psychoneuroimmunology Research, University of Rochester Medical Center, Rochester, New York.

Address reprint requests to: Mark R. Larson, PhD, The Center for PNI Research, Department of Psychiatry, Box PSYCH, University of Rochester Medical Center, 300 Crittenden Blvd., Rochester, NY 14642. Email: Mark_Larson{at}urmc.rochester.edu

OBJECTIVE: The primary objective of the present study was to identify neuroendocrine and immunological correlates of cardiovascular reactivity to an acute laboratory stressor.

METHODS: Subjects were 56 healthy volunteers. Heart rate and blood pressure were assessed at regular intervals during a 30-minute adaptation period and a 6-minute videotaped speech task. Blood was drawn before and after the task and was assayed for natural killer cell activity (NKCA), cortisol production, in vitro interferon gamma (IFN-) and interleukin 10 production by peripheral blood mononuclear cells (PBMC), and antibody titers to the Epstein-Barr virus. Psychological measures were also administered.

RESULTS: NKCA increased significantly in response to the task, and this increase was significantly and positively correlated with heart rate reactivity. IFN- production by PBMC also increased in response to the task, but these increases were unrelated to heart rate reactivity. In addition, baseline cortisol levels were found to be predictive of heart rate reactivity. Finally, questionnaire data were modestly related to various aspects of stress-induced reactivity.

CONCLUSIONS: Consistent with the task-related increases in NKCA and IFN-, acute stress may signal an increase in at least some aspects of the cell-mediated, or T_H1-driven, immune response. Furthermore, the finding that heart rate reactivity was related in part to baseline individual differences in cortisol production suggests that short-term cardiovascular responses to stress may be directly related to longer-term neuroendocrine modulation. Finally, the present results also help to highlight the influence of both sympathetic and nonsympathetic pathways in the response to acute stressors and suggest tentative links between certain psychological traits and various aspects of stress-induced reactivity.

Key Words: cardiovascular reactivity • natural killer cells • cytokines • cortisol • Epstein-Barr virus • psychoneuroimmunology.

Abbreviations: ANCOVA = analysis of covariance; AXS = Anger Expression Scale; DBP = diastolic blood pressure; EBV = Epstein-Barr virus; HR = heart rate; IFN- = interferon gamma; IL = interleukin; MCSDS = Marlowe-Crowne Social Desirability Scale; MMPI = Minnesota Multiphasic Personality Inventory; NKCA = natural killer cell activity; PBMC = peripheral blood mononuclear cells; SBP = systolic blood pressure; SNS = sympathetic nervous system; T_H = T helper (cell); TMAS = Taylor Manifest Anxiety Scale; TNF = tumor necrosis factor.

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