Stress and hypertension — a critical review

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.

Peripheral and brachial blood pressure during standardized occupation-related tests in normotensive and mild hypertensive men and women

“…Thus, the peripheral BP measurement is an additional possibility for assessment of the hyperreactivity which has been suggested as a pathophysiological mechanism in the development of cardiovascular diseases, especially of essential hypertension (Fredrikson 1991;Light et al 1992;Matthews et al 1993). The assessments in the literature of the clinical importance of hyperreactivity based on brachial BP can be seen to be contradictory (Freeman 1990;Rosenman and Hjemdahl 1991). In this context it is of interest to know whether brachial and peripheral BP react in the same way in normotensives and hypertensives when the body is faced with dierent kinds of demand.…”

Stress and hypertension: C and H type of hypertension and causes of resistance

“…Обов'язковим є також повторне обстеження пацієнта через 3-6 місяців після корекції факторів ризику і немедикаментозної терапії. При збереженні підвищеного рівня АТ (особливо коли підвищеним є середньодобовий АТ і відсоток підвищених показників становить > 25-30 %) вирішується питання про призначення медикаментозної терапії [72][73][74][75][76][77][78][79][80][81][82][83][84][85][86][87][88][89][90][91].…”