Effects of stressor controllability on acute stress responses : cardiovascular, neuroendocrine, and immune responses

This thesis is concerned with the effects of controllability over acute stressors on psychological and physiological responses intermediated by immune, cardiovascular, neuroendocrine systems. The effects of stressor controllability have been examined in animal studies based on the learned helplessness theory. However, there were few studies in human. Especially, there were remarkably few studies that examined the effects of stressor controllability on immunological system. In addition, results of these studies were inconsistent among researchers for methodological reasons. The present research was conducted to assess differences of physiological responses between two coping styles, namely passive coping and active coping, and to provide their psychophysiological evidence by using immune, cardiovascular, neuroendocrine indices. Based on previous findings out, hypothesis was that the active coping situation should elicit typical acute stress responses such as an increase of innate immunity and a decrease of acquired immunity. Furthermore, it was predicted that the active coping situation should have a greater impact on peripheral immune cells than a passive coping situation. This hypothesis was tested in experiment 1 that used a mental arithmetic task and a cold pressor task as active and passive coping situations respectively during which immune and cardiovascular responses were measured. As we predicted, under the active coping situation, innate immunity (natural killer (NK) cells) increased and acquired immunity (CD3 + T cells) decreased. Under the passive coping situation, immune responses were remarkably lower. The results suggest that immune responses under the active coping situation were evoked by increase of heart rate (HR) and blood pressure (BP) caused by adrenaline and noradrenaline. In contrast, those responses under the passive situation were elicited mainly by the increase of BP only caused by noradrenaline. For the experiment 2, the triadic-yoked design including controllable, uncontrollable, and control conditions were used according to typical animal study in literature. In addition, for manipulation of controllability, correct-error feedback to participants' answers was used during mental arithmetic task. III IV Contrary to the prediction, no effect of controllability was observed in any immune parameters, though the experimental manipulation of controllability was valid. This was explained by the fact that at the beginning of stressor exposure, stress responses of the active coping type were evoked regardless of stressor controllability. In addition, under 15 minutes of the uncontrollable stress situation, both active and passive coping responses were mixed degree of which is affected by individual difference. Thus, effects of uncontrollability might have been present as strong correlations between immune and cardiovascular reactivity, but not as a difference of mean values. The experiment 3 was designed to examine the time course of the uncontrollable acute stressor effect on immune responses up to 24 hours. For this purpose, participants performed four sessions of the acute stress task for two days. They performed mental arithmetic task under controllable or uncontrollable situations, and then performed again the same acute stress task several times, but under the controllable condition. Results supported hypothesis that the effects of an uncontrollable acute stressor should be present as the down-regulation of immune reactivity caused by inhibited cardiovascular and autonomic nervous responses. Among those participants who were exposed to the uncontrollable stressor in the first session, the increase of NK cells was lower than those in participants exposed to the controllable stressor. Especially, although the inhibition of immune activation in the uncontrollable condition did not appear in the first session, it appeared after the second session and became remarkable in the fourth session. In the final part of this thesis, the findings from the three experimental studies are combined to establish a new model concerning stressor controllability and acute stress response. With this new model, I discuss the possibility that the mechanism that down-regulate immune response to uncontrollable situation may one of the effective functions to adapt to the varying environment for survival.