Sympathetic Responses to Antihypertensive Treatment Strategies Implications for the Residual Cardiovascular Risk

Purpose of Review To examine whether and to what extent lifestyle, pharmacological and device-based therapeutic blood pressure lowering interventions are capable to restore a normal sympathetic cardiovascular function in hypertensive patients. Recent Findings Data collected by examining the results...

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Published inCurrent hypertension reports Vol. 27; no. 1; p. 21
Main Authors Dell’Oro, Raffaella, Quarti-Trevano, Fosca, Ambrosino, Pasquale, Grassi, Guido
Format Journal Article
LanguageEnglish
Published New York Springer US 23.07.2025
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ISSN1522-6417
1534-3111
1534-3111
DOI10.1007/s11906-025-01339-2

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Summary:Purpose of Review To examine whether and to what extent lifestyle, pharmacological and device-based therapeutic blood pressure lowering interventions are capable to restore a normal sympathetic cardiovascular function in hypertensive patients. Recent Findings Data collected by examining the results of more than 50 studies published during the past years by directly quantifying, via microneurography, the sympathetic nerve traffic responses to non-pharmacological and pharmacological antihypertensive treatment have shown that no normalization of the sympathetic cardiovascular function is achieved. Recently, a study by our group carried out in 219 hypertensive patients under monotherapy or combination drug treatment confirmed these results, by showing that, despite achieving an optimal blood pressure control, antihypertensive treatment fails to restore the normal sympathetic neural function detected in the normotensive healthy subjects. Summary The sympathetic nervous system plays a key role in blood pressure regulation and hypertension pathophysiology. Recent findings document its involvement also in determining the blood pressure lowering effects of antihypertensive agents. However, the available data show the inability to achieve during treatment a full sympathetic normalization, a finding which may represent one of the mechanisms responsible for the residual cardiovascular risk of the treated hypertensive patient.
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ISSN:1522-6417
1534-3111
1534-3111
DOI:10.1007/s11906-025-01339-2