Animal research suggests that oxytocin (OT) plays a role in stress responses and that in females, this role is modulated by estrogen. Yet little is known about the relation of OT to human stress responses. This study was conducted to examine the relations between estrogen activity and OT, identify stressors distinctively associated with elevations in OT, and investigate whether OT is related to cardiovascular and hypothalamic-pituitary-adrenocortical (HPA) activity in a laboratory challenge paradigm.
Seventy-three postmenopausal women who were on hormone therapy (HT) or not completed questionnaires assessing psychological distress and social relationships and then participated in a laboratory stress challenge (Trier Social Stress Task), during which OT, cortisol, and blood pressure were assessed.
HT was significantly associated with higher plasma OT. Controlling for HT, elevated plasma OT was significantly associated with gaps in social relationships, with less positive relationships with a primary partner, and with elevated cortisol levels. OT was not associated with stress reactivity or recovery.
In women, plasma OT signals relationship stress and is associated with elevated cortisol; it does not appear to significantly affect cortisol or blood pressure responses to acute stress.
OT = oxytocin; HPA = hypothalamic-pituitary-adrenocortical; HT = hormone therapy; TSST = Trier Social Stress Test; CAD = coronary artery disease; CHF = coronary heart failure; CRC = UCLA Clinical Research Center; BP = blood pressure; SCL-90 = Brief Symptom Inventory; PANAS = Positive and Negative Affect Schedule; RPM = rotations per minute; HLM = hierarchical linear modeling; GCA = growth curve analysis.
From the Department of Psychology (S.E.T.,G.C.G.) and Department of Geriatrics (P.H.,G.A.G.,T.E.S.), University of California, Los Angeles, Los Angeles, California; Department of Biobehavioral Health, Pennsylvania State University (L.C.K.).
Address correspondence and reprint requests to Shelley E. Taylor, UCLA Department of Psychology, 1282A Franz Hall, Los Angeles, CA 90095. E-mail: email@example.com
Received for publication October 4, 2004; revision received October 10, 2005.
This study was supported by an NSF grant (SBR 9905157) to the first author and by grants from the National Institute on Aging (AG10415 and AG17678). The second author was supported by an NIMH training grant (MH15750). Support for the conduct of the cortisol assays was provided by NIH grant M01 RR000080 to the UCLA GCRC.