The combined propranolol/TSST paradigm--a new method for psychoneuroendocrinology

Abstract

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.

Figure 1. Timeline of the testing procedure.

Figure 2. Effects of the TSST on the cortisol response in relation to the two experimental conditions: propranolol (n = 15) and placebo (n = 15).

Figure 3. Effects of the TSST on subjective stress ratings in relation to the two experimental conditions: propranolol (n = 15) and placebo (n = 15).

Figure 4. Effects of the TSST on the salivary alpha-amylase response in relation to the two experimental conditions: propranolol (n = 15) and placebo (n = 15).

Figure 5. Effects of the TSST on the heart rate in relation to the two experimental conditions: propranolol (n = 15) and placebo (n = 15).

Figure 6. Effects of the TSST on the heart rate in 1-minute intervals during and 5 minutes post-TSST in relation to the two experimental conditions: propranolol (n = 15) and placebo (n = 15).

Figure 7. Effects of the TSST on the diastolic blood pressure in relation to the two experimental conditions: propranolol (n = 15) and placebo (n = 15).

Figure 8. Effects of the TSST on the systolic blood pressure in relation to the two experimental conditions: propranolol (n = 15) and placebo (n = 15).