Douglas Mental Health University Institute, McGill University, Montreal, Quebec, Canada.
PLoS One. 2013;8(2):e57567. doi: 10.1371/journal.pone.0057567. Epub 2013 Feb 22.
Upon perception of a stimulus as stressful, the human brain reacts with the activation of the hypothalamus-pituitary-adrenal (HPA) axis and the sympathetic nervous system (SNS), to mobilize energy resources to better cope with the stressor. Since the perception of the stressor is the initial stimulus, a synchronicity between the subjective perception of stress and the physiological stress reactivity should be expected. However, according to a recent meta-analysis, these associations are weak and inconsistent. The goal of the current study was to investigate the interaction between the SNS, HPA and subjective stress perceptions, by introducing an experimental manipulation of this interaction. For this purpose, we combined the SNS inhibitor propranolol with the Trier Social Stress Test, and measured endocrinological and psychological responses to the stressor. Thirty healthy male participants were recruited and randomly assigned to either a propranolol (PROP; n = 15) or placebo (PLC; n = 15) group. All subjects were administered 80 mg of propranolol 60 minutes prior to exposure to psychosocial stress. Salivary cortisol and alpha amylase (sAA), heart rate, blood pressure and subjective stress responses were assessed throughout the study. We observed significantly reduced sAA levels and heart rate increases in the PROP group in response to stress, with no effects of the drug on systolic or diastolic blood pressure changes. In line with previous studies, a significant increase in cortisol was seen in response to the stress exposure. Importantly, the cortisol increase was significantly higher in the PROP group. A typical increase in subjective stress could be seen in both groups, with no significant group differences emerging. Complementing previous work, this study further demonstrates a significant interaction between the HPA and the SNS during acute stress. The HPA activity was found to be elevated in the presence of a suppressed SNS in reactivity to the TSST.
当人类感知到压力源时，大脑会通过激活下丘脑-垂体-肾上腺 (HPA) 轴和交感神经系统 (SNS) 来做出反应，调动能量资源以更好地应对压力源。由于对压力源的感知是最初的刺激，因此应该期望主观压力感知和生理压力反应之间存在同步性。然而，根据最近的一项荟萃分析，这些关联是微弱且不一致的。本研究的目的是通过引入对这种相互作用的实验操作来研究 SNS、HPA 和主观压力感知之间的相互作用。为此，我们将 SNS 抑制剂普萘洛尔与特里尔社会应激测试相结合，并测量了对压力源的内分泌和心理反应。我们招募了 30 名健康男性参与者，并将他们随机分配到普萘洛尔（PROP；n = 15）或安慰剂（PLC；n = 15）组。所有参与者在暴露于心理社会压力前 60 分钟给予 80 mg 普萘洛尔。在整个研究过程中，评估了唾液皮质醇和 alpha 淀粉酶（sAA）、心率、血压和主观压力反应。我们观察到，在应激反应中，PROP 组的 sAA 水平和心率显著降低，而药物对收缩压或舒张压变化没有影响。与之前的研究一致，皮质醇水平在应激暴露后显著增加。重要的是，PROP 组的皮质醇增加幅度明显更高。两组均可见典型的主观压力增加，但组间无显著差异。与之前的工作相补充，本研究进一步证明了 HPA 和 SNS 在急性应激期间的显著相互作用。在 HPA 活性被发现升高的情况下，SNS 受到抑制，对 TSST 的反应性增强。
