This article reviews key experimental studies concerning the possible contribution of behavioral stress to the development of primary hypertension. In animal preparations, chronic exposure to stressors in conjunction with predisposing genetic factors of high sodium/low potassium intake can lead to hypertension and cardiac pathology. Studies with human subjects are less definitive, but several lines of evidence suggest that high heart rate and blood pressure reactivity to behavioral stressors may indicate an increased susceptibility to hypertension, including an association between high reactivity and both borderline hypertension and a positive family history of hypertension, observations that stressors involving active coping evoke enhanced beta-adrenergic myocardial activity, resulting in cardiac output that is excessive relative to overall tissue oxygen consumption, and observations of decreased short-term sodium and fluid excretion during stressors in some individuals and an association between high salt intake and increased peak blood pressure levels evoked by exposure to stress. Indicated directions for future animal research include studies of the interactive effects of chronic stress with other environmental factors, such as high and low calcium intake, while in humans, future studies should incorporate monitoring of cardiovascular responses to real-life events, and should also include long-term follow-up investigations to evaluate more directly the predictive significance of high cardiovascular reactivity to stress.