This research was supported partially by the John D. and Catherine T. MacArthur Foundation, National Science Foundation Grant Nos. DBS-9211483 and SBR-9512459, National Institute of Aging Grant No. PO1-AG11585, National Institute of Mental Health Grant Nos. T32-MH19728 and T32-MH18831, and National Center for Research Resources Grant No. M01-RR00034.
Autonomic, Neuroendocrine, and Immune Responses to Psychological Stress: The Reactivity Hypothesisa
Article first published online: 7 FEB 2006
Annals of the New York Academy of Sciences
Volume 840, NEUROIMMUNOMODULATION: MOLECULAR ASPECTS, INTEGRATIVE SYSTEMS, AND CLINICAL ADVANCES pages 664–673, May 1998
How to Cite
CACIOPPO, J. T., BERNTSON, G. G., MALARKEY, W. B., KIECOLT-GLASER, J. K., SHERIDAN, J. F., POEHLMANN, K. M., BURLESON, M. H., ERNST, J. M., HAWKLEY, L. C. and GLASER, R. (1998), Autonomic, Neuroendocrine, and Immune Responses to Psychological Stress: The Reactivity Hypothesis. Annals of the New York Academy of Sciences, 840: 664–673. doi: 10.1111/j.1749-6632.1998.tb09605.x
- Issue published online: 7 FEB 2006
- Article first published online: 7 FEB 2006
Abstract: We examined the effects of brief psychological stressors on cardiovascular, neuroendocrine, and cellular immune response in 22 older women to investigate the common effects of stress across systems. Results revealed that psychological stressors heightened cardiac sympathetic activation, elevated plasma catecholamine concentrations, and affected the cellular immune response (ps < 0.05). In a replication and extension, 27 women caring for a spouse with a progressive dementia (high chronic stress) and 37 controls category matched for age and family income (low chronic stress) performed the 12-min laboratory stressor. Measures were taken before (low acute stress) and immediately following (high acute stress) exposure to the laboratory stressors as well as 30 min after termination of the stressor (recovery period). Acute stress again heightened cardiac sympathetic activation, elevated plasma catecholamine concentrations, and affected cellular immune responses (ps < 0.05), whereas chronic stress was associated with higher reports of negative affect, enhanced cardiac sympathetic activation, elevated blood pressure and plasma levels of ACTH, and diminished production of interleukin-1β (ps < 0.05). Correlational analyses in both studies further suggested that individuals who showed the greatest stress-related changes in HPA activation also exhibited the greatest diminution in cellular immune response.