Evaluation of the mechanisms underlying the vascular dysfunction induced by restraint stress

Abstract

Physical or psychological stress is defined as a state of disharmony or threat to homeostasis that may be caused by psychological, environmental or physiological stressors. Several studies show that physical, as well as psychological stress, contributes to the development of cardiovascular diseases such as hypertension. Therefore, stress causes significant changes in circulatory function, appearing as an important risk factor for the development of cardiovascular diseases. Some studies have suggested a myogenic mechanism in which stress alters the vascular reactivity inducing increased vascular responses to vasoconstrictors agents and reduced relaxation to vasodilating agents, further suggesting that stress induces endothelial dysfunction. The latter is defined as an imbalance in the synthesis, release or effect of endothelial relaxing factors such as nitric oxide (NO). The increase of oxidative stress is also an important mechanism that contributes to endothelial dysfunction. The reactive oxygen species (ROS) such as superoxide anion (O2-) oxidize biomolecules initiating lipid peroxidation, which leads to cardiovascular dysfunction. It is important to note that stress increases ROS production. Therefore, the hypothesis of this study is that acute stress stimulates the production of ROS in the vasculature and this response would lead to vascular dysfunction with consequent alterations in vascular reactivity, reduced bioavailability of NO and increased blood pressure. Therefore, the aim of this study is to evaluate the mechanisms underlying the vascular dysfunction induced by acute stress.