Prehypertension and stress reactivity Medeiros RF et al. following an exercise bout. However, West et al.32 observed a significant reduction in the total vascular resistance during mental stress in subjects with borderline HT after an exercise bout. In this context, the present study adds the finding that the forearm vasodilator response during mental stress was enhanced after an acute bout of exercise in subjects with PHT, which suggests that there was enhanced vasodilation in the forearm skeletal muscles. Three primary mechanisms might be involved in the enhanced vasodilation in response to mental stress in skeletal muscles following an acute bout of exercise. First, it was observed that the exercise bout reduced SBP at rest in subjects with PHT, which might have attenuated the passive arterial distension caused by increased perfusion pressure27 and thus might be associated with the reduction in baseline blood flow. However, regardless of the cause, reduced baseline blood flow increases the vasodilator reserve, thereby facilitating vasodilation during mental stress. Second, there is evidence that following a bout of dynamic exercise, endothelial-dependent vasodilation is improved, even in vascular bed segments that were not directly involved in the exercise.12,33 This phenomenon has been attributed to a systemic increase in the expression and phosphorylation of endothelial nitric oxide synthase34,35 as a consequence of the systemic increase in shear stress during exercise, which leads to an increase in the bioavailability of NO.33 In addition, it was shown that beta 2- adrenergic receptor responsiveness is enhanced after an acute bout of exercise,36 which can also improve the vasodilator response to mental stress. Third, Brownley et al.36 showed that a reduced noradrenaline response to a stress task was associated with an attenuated post-exercise stress-related blood pressure response. Therefore, it is possible that a reduction in sympathetic vasoconstrictor activity might also have contributed to this effect. The results of this study have some clinical implications. The novel result of this study is that a single bout of exercise reversed an impaired vasodilator response to mental stress, as indicated by a lower blood pressure increase. Considering that an enhanced blood pressure response to mental stress is associated with a greater risk for the development of cardiovascular disease, our results suggest that by correcting the vasodilator response to mental stress, as the exercise bout did, it is possible to attenuate the blood pressure increase during mental stress in subjects with PHT. Further studies should determine whether chronic exposure to exercise leads to vascular adaptations that correct the vasodilator response, and whether other non-pharmacolo- gical vasodilatory interventions such as anti-oxidant and/or L-arginine supplements would yield similar benefits. The results presented here should be interpreted con- sidering certain limitations. Blood flow was measured by venous occlusion plethysmography, which takes into account the blood flow to all tissues in the evaluated segment. The tissue that contributes most to the total blood flow measured by plethysmography is skeletal muscle,37 but skin blood flow can also contribute to the results to a small extent.37 Therefore, the temperature in the experi- mental room was maintained at a fairly constant level to minimize variations in skin blood flow. This technique has been validated,38 and is widely used to measure blood flow in skeletal muscle. It is possible that repeated exposure to mental stress could lead to habituation. However, Hammer et al. showed that repeated exposure to the same test that 1528 CLINICS 2011;66(9):1523-1529 was used in the present study did not change cardiovas- cular responses to mental stress.39 In addition, in the present study, there was no change in stress perception scores before and after exercise in either group. Hence, a repeated exposure to mental stress might not have influenced the results that were observed in the present study. Another limitation is the low number of men in the sample. This limitation is minimal because there was no significant difference in the number of men between the groups. Finally, we used a maximal dynamic exercise test to investigate the effects of exercise on cardiovascular responses to mental stress. This method has the advantage of providing a standardized exercise stimulus. It was shown previously that a bout of maximal dynamic exercise increases endothelial-mediated vasodilation for at least 60 minutes12 and increases the systemic production of NO,33 which supports our study mechanistically. However, this exercise protocol is not used during training programs. Thus, further studies should investigate whether a regular session of aerobic exercise training yields similar benefits in subjects with PHT. CONCLUSION The present study showed that subjects with PHT have elevated blood pressure and blunted vasodilation during mental stress compared with subjects with NT, and a single bout of maximal dynamic exercise reduced their blood pressure and normalized their vasodilator response to mental stress. ACKNOWLEDGMENTS The authors thank Felipe de Sa´ Pereira, Thales Coelho Barbosa, Tatiane Marinz de Souza and Roge´rio Barbosa M. Barros for their assistance during the experiments and Labs D’OR for biochemical blood analyses. REFERENCES 1. 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