The impact of acute mental stress on brachial artery flow-mediated dilation in women diagnosed with depression.

Endothelial function, assessed by flow-mediated dilation (FMD), may be transiently attenuated in healthy adults following acute mental stress. However, the impact of acute mental stress on endothelial function in the context of clinical depression is unknown. This study examined the impact of acute mental stress on FMD in women with a diagnosis of a depressive disorder. Forty-three otherwise healthy women (33 ±â€¯14 years) participated. Brachial artery diameter and blood velocity were assessed with ultrasound. FMD was assessed immediately prior to and 15 min following the Trier Social Stress Test (TSST). The FMD protocol included 5 min of forearm cuff occlusion (pressure = 250 mm Hg), followed by release. Shear stress was estimated by calculating shear rate (SR = brachial artery blood velocity/diameter). Stress reactivity was assessed via changes in mean arterial pressure (MAP), heart rate (HR) and salivary cortisol. Results are mean ±â€¯SD. A significant stress response was elicited by the TSST [MAP, HR and salivary cortisol increased (p < 0.05)]. Neither the SR stimulus nor FMD response differed pre-versus post-stress (p = 0.124 and p = 0.641, respectively). There was a modest negative correlation between cortisol reactivity and change in FMD from pre- to post-stress (R = -0.392, p = 0.011). To conclude, acute mental stress did not consistently impair endothelial function in women diagnosed with a depressive disorder; however, higher cortisol reactivity may increase the likelihood of post-stress endothelial dysfunction. Further research is required to better understand the factors influencing the relationship between acute mental stress, cortisol and endothelial function in women with depression.

The influence of vitamin C on the interaction between acute mental stress and endothelial function.

PURPOSE: To determine whether orally administered vitamin C attenuates expected mental stress-induced reductions in brachial artery endothelial function as measured by flow-mediated dilation (FMD). METHODS: Fifteen men (21 ± 2 years) were given 1000 mg of vitamin C or placebo over two visits in a randomized, double-blinded, within-subject design. Acute mental stress was induced using the Trier Social Stress Test (TSST). Saliva samples for cortisol determination and FMD measures were obtained at baseline, pre-TSST, and 30 and 90-min post-TSST. An additional saliva sample was obtained immediately post-TSST. Cardiovascular stress reactivity was characterized by changes in heart rate (HR) and mean arterial pressure (MAP). RESULTS: A significant stress response was elicited by the TSST in both conditions [MAP, HR, and salivary cortisol increased (p < 0.001)]. Overall FMD did not differ pre- vs. post-stress (time: p = 0.631) and there was no effect of vitamin C (condition: p = 0.792) (interaction between time and condition, p = 0.573). However, there was a correlation between cortisol reactivity and changes in FMD from pre- to post-stress in the placebo condition (r 2 = 0.66, p < 0.001) that was abolished in the vitamin C condition (r 2 = 0.02, p = 0.612). CONCLUSION: Acute mental stress did not impair endothelial function, and vitamin C disrupted the relationship between cortisol reactivity and changes in FMD post-stress. This suggests that acute mental stress does not universally impair endothelial function and that reactive oxygen species signaling may influence the interaction between FMD and stress responses.