Prehypertension and stress reactivity Medeiros RF et al. CLINICS 2011;66(9):1523-1529 Figure 1 - Absolute hemodynamic responses to mental stress, adjusted for gender, before and after an exercise bout in subjects with prehypertension or normotension. Values are the mean ¡ SEM. *, p,0.05 vs. within-group baseline; {, p,0.05 vs. same condition between groups; {, p,0.05 vs. before-exercise within group. endpoint of the present study. Moreover, the DBP and MBP percent change values in the NT group decreased compared with the values obtained before the exercise bout, which was not observed in the PHT group. DISCUSSION The present study investigated hemodynamic responses to a mental stress test performed before and after a bout of maximal dynamic exercise in subjects with PHT or NT. The hypothesis of this study was that subjects with PHT and NT have different levels of vascular reactivity to mental stress and that this difference would disappear after a bout of exercise. This approach revealed two major findings. First, subjects with PHT had higher blood pressure during mental stress than subjects with NT, and the exercise bout reduced their blood pressure during the mental stress test. Second, subjects with PHT presented a blunted vasodilator response to mental stress, and the exercise bout normalized this response. Previous studies have also shown elevated blood pressure levels during mental stress in subjects with PHT.6-8 However, the mechanisms that mediate this phenomenon are still unclear. Schwartz et al.7 and the present study found that heart rate increases during mental stress were similar in subjects with PHT versus those with NT. However, no study has yet determined whether the increased stroke volume and cardiac output during mental stress are enhanced in subjects with PHT. Therefore, it is possible that increased cardiac output in response to mental stress might contribute to the augmented blood pressure levels in subjects with PHT. 1526 Santangelo et al.6 and Schwartz et al.7 found that part of the enhanced pressor response to mental stress in subjects with PHT was associated with blunted forearm vasodila- tion. In addition, Scharwrtz et al.7 showed that blunted vasodilation in response to mental stress in subjects with PHT was not mediated by sympathetic nerve activity in the muscle. In the present study we also observed an attenuated forearm vasodilator response to mental stress, which corroborates previous findings. Subjects with PHT had a higher blood flow and vascular conductance at rest, which reduced their vasodilator reserve (i.e., the change from baseline to maximal vasodilation), thus impairing their vasodilator response to mental stress. A reduction in the vasodilator reserve was shown previously in the forearm7 and coronary25 circulation of subjects with PHT, and this reduction seems to be partially mediated by passive arterial distention as a consequence of increased perfusion pressure.26 Additionally, this mechanism seems to present at the onset of HT pathophysiology.27 Further evolution of the disease induces arterial remodeling to decrease the tensile stress in the arterial wall,27 which occurs by means of an increase in the intima-media thickness and a decrease in the vessel lumen.26 The increased blood flow in the muscle vascular bed during mental stress is dependent on the integrity of the vascular endothelium, and nitric oxide (NO) production by the endothelium seems to be a cornerstone mechanism. Studies have shown that during mental stress, sympathetic cholinergic fibers,4 beta 2-adrenergic receptor stimulation by adrenaline28,29 and increased shear stress30 stimulate the release of NO, leading to vasodilation. Thus, when