Chronic stress in the development of essential hypertension, role of rilmenidine in the treatment of stress induced hypertension

Hypertension is an independent risk factor of cardiovascular diseases. Several factors contribute to its development, including chronic stress, which may induce hypertension by increasing sympathetic activity. The signs of increasing sympathetic activity can be primarily detected in the initial phase of hypertension, which is characterized by the increase in cardiac output. In addition to the hemodynamic consequences (increase in cardiac output, tachycardia, coronary vasoconstriction, proarrhythmia), the increase in sympathetic activity has many harmful effects. Numerous metabolic (insulin resistance, dyslipidemia), structural and trophic effects (endothelial dysfunction, vascular hypertrophy, myocardial hypertrophy), as well as thrombotic and humoral processes (procoagulation, enhancement of thrombocyte aggregation, sodium retention, activation of the renin-angiotensin-aldosterone axis) may develop and consequently damage body functions at many targets. Several different antihypertensive drug classes are available for reducing increased sympathetic activity, including peripheral alpha and beta blockers and compounds with central effects. First generation antihypertensive drugs with central mechanisms of action (e.g. clonidine, guanfacine, alpha-methyldopa) is currently rarely administered and only for a few indications as they have a significant adverse events profile. Among second generation compounds with central effects, rilmenidine stimulates imidazoline-1 receptors and thus beneficially influences mild or moderate hypertension that involves enhanced sympathetic nervous system activity.