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This thesis explored whether haemodynamic responses to psychological stress test predict future blood pressure (BP) levels: the Reactivity Hypothesis. The research included a systematic review and two prospective cohort studies in the UK and Thai samples. In addition, the Blunted Reactivity Hypothesis, which posits that cardiovascular reactivity is inversely related to symptoms of anxiety and depression, was examined in cross-sectional analyses. A systematic review with meta-analysis and meta-regression with 41 prospective cohort studies (from 1950 to 2012) examined whether cardiovascular responses to psychological stress tests predict future BP levels, hypertension status, preclinical coronary heart disease (CHD) and cardiac events. Three possible moderators were included in analyses: type of task (active versus passive coping), age group (children versus adults), and duration of follow-up (short versus long-term follow-up). The review found that systolic BP reactions to psychological stress tests predict future systolic BP levels and that there was better prediction in child samples with shorter follow-up periods. Similarly, diastolic BP reactions to psychological stress predicted future diastolic BP levels. Cardiovascular reactions to psychological stress tests did not predict hypertension, preclinical CHD, or cardiac events. Cross-sectional analysis of two studies conducted in the UK and Thailand provided some evidence that anxiety and depressive symptoms were negatively associated with cardiovascular reactivity: these findings supported the Blunted Cardiovascular Hypothesis. However, these relationships were observed in the UK sample, but not in the Thai sample. Further, Thai participants responded to psychological stress task with large cardiovascular reactions, of a similar magnitude to the UK participants and observed in previous studies of Europeans and North Americans. Finally, prospective analyses revealed that systolic BP responses to mental arithmetic predict future systolic BP levels after one year of follow-up in both UK and Thai individuals, after controlling for baseline cardiovascular activity and traditional risk factors. In contrast, haemodynamic responses did not predict future BP. These results provide support for the “Reactivity Hypothesis” although the effect sizes were relatively small. However, responses to only one of the three stressors, mental arithmetic, predicted future BP implicating beta-adrenergically mediated cardiovascular responses. However, there was no physiologic evidence (i.e., cardiac output responses) that suggested beta-adrenergic mechanisms. Accordingly, future studies should examine alternate mechanisms (e.g., platelet aggregation and endothelial function) and cardiovascular responses in larger samples with a longer follow-up to further clarify the predictive value of reactivity in the development of hypertension, along with potential mechanisms.