Observations on the adverse effect of chronic environmental stress on blood pressure in individuals, and the incidence of hypertension in populations, have raised the possibility that aberrant physiological responses to stressful stimuli may play a role in the development of human hypertension. A variety of investigations, both clinical and experimental, have been conducted to explore a neurogenic dimension in the pathogenesis of hypertension. Reactivity is defined as the change in blood pressure, heart rate, or other hemodynamic parameters in response to physical or mental stimuli. Data from clinical studies have shown that reactivity is a stable measurement within individuals. Augmented reactivity is observed in patients with hypertension compared with normotensive subjects, and can also be detected in the young, often associated with other risk factors for hypertension. Racial differences in reactivity have been shown, with enhanced vascular reactivity observed among blacks compared with greater cardiac reactivity in whites. Neither stress, nor reactivity to stress has been shown to have a causal role in the development of hypertension. Although augmented stress-induced reactivity is strongly associated with groups having a greater risk for future hypertension, the role that reactivity plays in this process remains to be delineated.