Abstract
The review presents a modern view on stress as a risk factor for the development of arterial hypertension (AH). A variety pathogenic mechanisms responsible for increase of blood pressure during stress exposure are described in detail. The importance of the sympathetic activation as a key link in the development of stress-induced AH and initiation of a cascade of pathophysiological reactions that realize their adverse effects at the level of the whole organism is underlined. Particular attention is paid to worksite AH as a variant of stress-induced hypertension due to its wide prevalence and association with an increased risk of cardiovascular complications, primarily myocardial infarction and stroke. Epidemiological data and results of recent metanalysis are presented, indicating the high significance of job strain as a risk factor for adverse cardiovascular events. The actual psychological stress reduction programs are described. Possibilities of using β-blockers in patients with stress-induced hypertension as drugs affecting the central pathogenetic trigger of this disease are considered. The advantages of using bisoprolol as a highly selective β-blocker are considered taking into account the available body of evidence for its effectiveness in patients with worksite AH, as well as its metabolic neutrality and target-organ protective properties.
Highlights
The review presents a modern view on stress as a risk factor for the development of arterial hypertension (AH)
A variety pathogenic mechanisms responsible for increase of blood pressure during stress exposure are described in detail
The importance of the sympathetic activation as a key link in the development of stress-induced AH and initiation of a cascade of pathophysiological reactions that realize their adverse effects at the level of the whole organism is underlined
Summary
В исследованиях показано, что у пациентов мужского пола с высоким риском развития АГ во время психологического стресса наблюдаются существенно более высокие показатели как АД, так и системного сосудистого сопротивления. При длительном, часто повторяющемся воздействии стрессоров возникает дизрегуляция автономной нервной и гипоталамо-гипофизарно-надпочечниковой систем с повышенным выбросом ими гормонов адаптации, что в итоге ведет к повышению АД, причем такая гипертоническая реакция имеет место не только непосредственно во время действия провоцирующего фактора, но и сохраняется в течение определенного времени после его элиминации [25].
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