Does administration of vitamin C attenuate an acute mental-stress induced impairment in endothelial function?

Abstract

Acute mental stress has been shown to elicit a transitory impairment in the function of the endothelial cells that line the arteries. While this effect of mental stress on endothelial function is generally accepted, the mechanisms by which this occurs remain unclear. One putative mechanism is the generation of reactive oxygen species (ROS). The objective of the study performed for this thesis was to examine whether orally administered vitamin C (an antioxidant which can combat the negative effects of ROS) can attenuate reductions in brachial artery endothelial function due to mental stress. Fifteen men (21 ± 2 yrs) were given 1000mg of vitamin C or placebo over two experimental days (one per visit) in a randomized, double-blinded, within-subject study. Acute mental stress was induced using the Trier Social Stress Task (TSST), which consists of both a speech and mental arithmetic task. Flow-mediated dilation (FMD), an index of endothelial function, was assessed using ultrasound at baseline, prior to the acute mental stress task, and 30, and 90 minutes post-stress. Saliva samples were taken to measure the stress hormone cortisol at all FMD time points as well as immediately post-stress. Stress reactivity was also characterized by changes in heart rate (HR) and mean arterial pressure (MAP). A significant stress response was elicited by the TSST in both conditions as MAP, HR and salivary cortisol all increased significantly. Contrary to the hypothesis, endothelial function was unaffected by time (p = 0.631) or condition (p = 0.792). However, a correlation was found between Δ%FMD at 30 minutes and ΔMAP (p = 0.015) and Δsalivary cortisol (p < 0.001) in the placebo condition but not the vitamin C condition (p = 0.480, p = 0.461). These findings indicate that acute mental stress may not impair endothelial function in healthy, young adults. The observation that relationships between stress reactivity parameters and changes in FMD were abolished in the vitamin C condition may indicate that ROS signaling influences FMD post-stress. Further research is required to elucidate the role of ROS in modulating stress-induced changes in endothelial function.