ABSTRACT
Recurrent psychosomatic stress has been popularly thought to cause permanent hypertension by repeated reactive blood pressure elevations. These are considered by some to be caused by various mechanisms, including an increased sympathetic outflow and a decreased parasympathetic inhibition, or possibly an inborn functional abnormality in the walls of the resistance vessels, which becomes a structural abnormality as a result of the elevated pressure. Recent work, however, has questioned some of these concepts. Many of the assumptions in the past concerning the ill-effects of elevated blood pressure have been based on clinic or office readings. With the more widespread use of ambulatory monitoring, first developed in the 1960s, information has accumulated which has helped to clarify the predictive value of such office readings. Ambulatory monitoring has also given much information about the relationship between daily activities, blood pressure reactivity and the mean daily blood pressure level. It appears that only the mean daily level is related to cardiovascular morbidity and mortality. Variations in blood pressure in response to bodily and mental activity are not so related. Nor has it been shown that variability is a precursor of fixed hypertension. The role of laboratory stressors is discussed to see whether they are predictive of future hypertension and whether they reflect real life situations. Clinical studies of the relationship between stress and hypertension and, in particular, specific causes of stress such as anxiety and hostility are considered. It is concluded that there is no satisfactory evidence that psychosocial stress leads to the elevation of the mean daily blood pressure with its pathogenic connotations.
