The role of mental stress in the development of hypertension and coronary heart disease remains uncertain. Its effects are likely to depend on an interaction of at least three factors: the nature of the stressor, its perception by the individual, and the individual's physiological susceptibility. This type of interaction is supported by animal studies. Most experimental studies in man have measured the cardiovascular response to acute laboratory stressors, on the assumption that subjects showing greater reactivity are at higher risk of developing cardiovascular disease. Experimental support for this "reactivity hypothesis" is limited, and the technique suffers from a number of limitations, such as an emphasis on acute rather than chronic effects, and a doubtful relevance to real-life stressors. It is possible, however, that transient surges of autonomic activity occurring in response to behavioral stimuli could trigger acute cardiac events. The role of environmental stressors can be studied by ambulatory monitoring techniques. Using the Karasek Job Content Survey (a known predictor of coronary heart disease), we have found that men in high strain jobs (defined by a combination of high demands and low control) are more likely to be hypertensive, and to show left ventricular hypertrophy than men in less stressful jobs. © 1990 Springer-Verlag.