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Am J Hypertens. 2010 Oct;23(10):1052-60. doi: 10.1038/ajh.2010.154. Epub 2010 Jul 22.

Sympathetic neural activity in hypertension and related diseases.

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Clinica Medica, Ospedale San Gerardo dei Tintori, Università Milano-Bicocca, Italy.



Several hemodynamic variables, such as blood pressure, vascular resistance, cardiac output, and heart rate, are regulated, among others, by sympathetic cardiovascular influences. This has led many years ago investigators to advance the hypothesis that alterations in the sympathetic modulation of the cardiovascular system may occur in hypertension and related disease.


The role of the sympathetic nervous system as promoter and amplifier of the hypertensive state has been examined in a consistent number of studies carried out by making use of sophisticated and sensitive approaches to evaluate adrenergic function, such as the norepinephrine spillover technique and the recording of efferent postganglionic muscle sympathetic-nerve traffic.


The results of the above-mentioned investigations support the concept that adrenergic activation characterizes essential hypertension, correlating with the clinical severity of the disease. Furthermore, sympathetic cardiovascular influences may favor the hypertensive disease progression, by concurring with other hemodynamic and nonhemodynamic factors at the development of target organ damage. Finally, an adrenergic overdrive of pronounced degree also characterizes hypertension-related cardiovascular and metabolic disease. In several of these clinical conditions, the adrenergic overdrive plays a role in the disease's physiopathology and prognosis.


The data reviewed in this article provide evidence that sympathetic activation represents a hallmark of the essential hypertensive state. They further show that adrenergic neural factors may participate at the development and progression of the hypertensive state and its complications. This represents the rationale for the use of antihypertensive and, in more in general, cardiovascular drugs capable to exert sympatho-inhibitory effects.

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