Abstract
Autonomic cardiovascular control is impaired in hypertension, leading to a reduction in the parasympathetic and to an increase in the sympathetic influences to the heart and peripheral vessels. The sympathetic dysfunction depends on a variety of reflex and non-reflex mechanisms and participates at development and progression of the complex cardiometabolic alterations, known as “end-organ damage”, detectable in the clinical course of hypertensive disease. This paper will review the main features of the adrenergic abnormalities characterizing essential hypertension, the mechanisms potentially involved in this neural abnormality, its consequences as well as potential reversibility by non-pharmacological as well as pharmacological interventions.
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