From the Department of Psychology and Neuroscience (MacCormack, Gaudier-Diaz, Lindquist, Muscatell), University of North Carolina at Chapel Hill, Chapel Hill, North Carolina; Department of Psychiatry (MacCormack), University of Pittsburgh, Pittsburgh, Pennsylvania; Graduate School of Education (Armstrong-Carter), Stanford University, Stanford, California; Department of Psychiatry (Meltzer-Brody), University of North Carolina at Chapel Hill, Chapel Hill, North Carolina; Monash Institute of Pharmaceutical Sciences, Drug Discovery Biology Theme (Sloan), Monash University, Parkville; Division of Surgery (Sloan), Peter MacCallum Cancer Center, Melbourne, Victoria, Australia; Lineberger Comprehensive Cancer Center (Muscatell) and Carolina Population Center (Muscatell), University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Psychosom Med. 2021;83(9):959-968. doi: 10.1097/PSY.0000000000001009.
β-Adrenergic receptor signaling, a critical mediator of sympathetic nervous system influences on physiology and behavior, has long been proposed as one contributor to subjective stress. However, prior findings are surprisingly mixed about whether β-blockade (e.g., propranolol) blunts subjective stress, with many studies reporting no effects. We reevaluated this question in the context of an acute psychosocial stressor with more comprehensive measures and a larger-than-typical sample. We also examined the effects of β-blockade on psychophysiological indicators of sympathetic and parasympathetic nervous system reactivity, given that β-blockade effects for these measures specifically under acute psychosocial stress are not yet well established.
In a double-blind, randomized, placebo-controlled study, 90 healthy young adults received 40 mg of the β-blocker propranolol or placebo. Participants then completed the Trier Social Stress Test, which involved completing an impromptu speech and difficult arithmetic in front of evaluative judges. Self-reported emotions and appraisals as well as psychophysiology were assessed throughout.
Propranolol blunted Trier Social Stress Test preejection period reactivity (b = 9.68, p = .003), a marker of sympathetic nervous system activity, as well as salivary α-amylase reactivity (b = -0.50, p = .006). Critically, propranolol also blunted negative, high arousal emotions in response to the stressor (b = -0.22, p = .026), but cognitive appraisals remained intact (b values < -0.17, p values > .10).
These results provide updated experimental evidence that β-adrenergic blockade attenuates negative, high arousal emotions in response to a psychosocial stressor while also blunting sympathetic nervous system reactivity. Together, these findings shed light on the neurophysiological mechanisms by which stressors transform into the subjective experience we call "stress."Trial Registration: ClinicalTrials.gov Identifier: NCT02972554.
β-肾上腺素能受体信号转导是交感神经系统对生理和行为影响的关键介质，长期以来一直被认为是主观应激的一个贡献因素。然而，先前的研究结果令人惊讶地不一致，即β-阻断剂（如普萘洛尔）是否能减轻主观应激，许多研究报告没有效果。我们在急性心理社会应激的背景下，用更全面的测量方法和比典型样本更大的样本量重新评估了这个问题。我们还研究了β-阻断剂对交感和副交感神经系统反应的生理指标的影响，因为β-阻断剂对这些指标在急性心理社会应激下的具体作用尚未得到很好的证实。
在一项双盲、随机、安慰剂对照研究中，90 名健康的年轻成年人接受了 40 毫克的β-阻断剂普萘洛尔或安慰剂。然后，参与者完成了特里尔社会应激测试，其中包括在评估者面前完成即兴演讲和困难的算术。在整个过程中评估了自我报告的情绪和评价以及生理心理学。
普萘洛尔减弱了特里尔社会应激测试的射血前期反应性（b = 9.68，p =.003），这是一种交感神经系统活动的标志物，以及唾液α-淀粉酶反应性（b = -0.50，p =.006）。重要的是，普萘洛尔也减轻了应激源引起的负面、高唤醒情绪（b = -0.22，p =.026），但认知评价保持不变（b 值< -0.17，p 值>.10）。
这些结果提供了更新的实验证据，表明β-肾上腺素能阻断减弱了对心理社会应激的负面、高唤醒情绪的反应，同时也减弱了交感神经系统的反应性。这些发现共同揭示了应激源转化为我们称之为“应激”的主观体验的神经生理机制。试验注册：ClinicalTrials.gov 标识符：NCT02972554。
