β-Adrenergic Contributions to Emotion and Physiology During an Acute Psychosocial Stressor

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.