[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 centrally acting
drugs. 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
centrally acting, second generation drugs, rilmenidine stimulates imidazoline-I1
receptors and thus beneficially influences mild or moderate hypertension that involves
enhanced sympathetic nervous system activity.]
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