Abstract
The past 30 years have seen a “renaissance” of the interest of investigators and clinicians for the possible contribution of sympathetic neural factors at the development and progression of essential hypertension [1]. This growing interest is based on a long series of findings and evidence. For brevity, they can be summarized as follows. First, it has been repeatedly shown that sympathetic neural factors are already activated in the early phases of hypertension and sometimes even in the prehypertensive states when blood pressure values are still in the high-normal range [1]. Second, it has been convincingly reported that adrenergic overdrive may parallel the blood pressure elevation and participate at the pathogenesis of end-organ damage [1]. Finally, results of some recent studies and clinical trials have suggested that in some forms of essential hypertension, such as resistant hypertension, therapeutic interventions capable to obtain a sympathetic denervation at the level of the kidney may trigger blood pressure lowering effects, thus reducing the very high cardiovascular risk of patients with elevated blood pressure levels resistant to three or more antihypertensive drugs (including a diuretic) administered at full daily dosage [2].
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Grassi, G., Seravalle, G., Dell’Oro, R. (2015). Neurogenic and Non-neurogenic Mechanisms of White-Coat Hypertension. In: White Coat Hypertension. Springer, Cham. https://doi.org/10.1007/978-3-319-07410-8_3
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DOI: https://doi.org/10.1007/978-3-319-07410-8_3
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