International Journal of Hypertension for the variable predictive response to laboratory stress tests is unclear. The inconsistency may be a consequence of the type of stressors used [4, 5, 38, 39] and the interaction of psychosocial factors with blood pressure response to the stressor [40–42]. Psychological stress tests may be better than cold pressor stress tests at predicting future cardiovascular events [4, 5, 22, 43, 44]. This diﬀerential eﬀect of stressor type and hypertension development may be a consequence of diﬀerential psychosocial factor interaction with stressors. In a study of a European population, psychosocial factors appear to have a greater impact on reactivity to cold pressor than reactivity to mental stress [16]. Our study compares the impact of anxiety on reactivity to cold pressor and anger recall in African Americans. Anxiety was signiﬁcantly asso- ciated with blood pressure response to both stressors in this population. Another explanation for the inconsistent ﬁndings of increased risk of hypertension development with increased reactivity is the interaction of psychosocial factors with car- diovascular reactivity to promote hypertension develop- ment. For example, studies show that hostility, depression, and anger contribute to increased reactivity [40, 45, 46]. Psychosocial factors also are associated with increased in- cidence of cardiovascular events [47–50] as well as the de- velopment of cardiovascular disease [51, 52]. We show that the psychosocial factor, anxiety, can inﬂuence the reactivity response to acute stress. However, because the study design was cross-sectional, it could not be determined whether state anxiety interaction with cardiovascular response to acute stress predicts hypertension development. This study shows that the current state of anxiety was signiﬁcantly associated with blood pressure response to laboratory stress tests. Consequently, anxiety levels should be assessed when using acute laboratory stress tests for iden- tiﬁcation of those with increased cardiovascular reactivity. Further studies are needed to determine whether reactivity normalized to anxiety increases the accuracy in identifying hyperresponders and, subsequently, predicting future hyper- tension development. 6. Limitations The small sample size is a major limitation of this study. These ﬁndings need to be validated in a larger cross sectional population of African Americans. Additionally, our study design did not allow us to determine whether the impact of anxiety on blood pressure response to acute stressor is unique to anxiety or whether other psychosocial factors similarly in- ﬂuence blood pressure response to acute stress in our cohort. Another limitation of the study is that adrenergic system activation was not measured; consequently, it could not be determined if the two stressors diﬀerentially activated the beta or alpha-adrenergic receptor pathways. This informa- tion would be helpful in future longitudinal studies that will address how activation of the alpha and beta adren- ergic receptors pathways ultimately leads to hypertension development and the attending cardiovascular disease. A longitudinal study design will also help to address the ques- 5 tion of whether inclusion of anxiety enhances the ability of increased reactivity to predict future elevations of blood pressure. Conﬂict of Interests The authors declare that there is no conﬂict of interests. Acknowledgements The authors thank Dr. Redford Williams of Duke University School of Medicine for his guidance. 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