Abstract
Hyperactivation of the sympathetic nervous system (sympathetic overdrive) is the central mechanism for the development of arterial hypertension. Among antihypertensive drugs, only beta-blockers without internal sympathetic activity, for example, bisoprolol, provide complete control of sympathetic hyperactivation. Highly selective β1-adrenergic blockers inhibit sympathetic activity in the heart and kidneys, preserving β2-mediated vasodilation and reducing the risk of adverse effects due to β2-receptor blockade in the lungs and peripheral tissues.
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