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(Hypertension. 2007;49:5.)
© 2007 American Heart Association, Inc.

Editorial Commentaries

Adrenergic Overdrive as the Link Among Hypertension, Obesity, and Impaired Thermogenesis

Lights and Shadows

Guido Grassi

From the Clinica Medica, Dipartimento di Medicina Clinica e Prevenzione and Dipartimento di Statistica, Università Milano-Bicocca, Ospedale San Gerardo, Milan, Italy; Istituto Auxologico Italiano, Milan, Italy; Centro Interuniversitario di Fisiologia Clinica e Ipertensione, Milan, Italy.

Correspondence to Guido Grassi, Clinica Medica, Ospedale S. Gerardo, Via Pergolesi 33, 20052 Milan, Italy. E-mail guido.grassi@unimib.it

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The sympathetic nervous system plays a pivotal role in both blood pressure and metabolic homeostatic control by regulating cardiac output, peripheral vascular resistance, heat production, and resting metabolic rate, which accounts for a large fraction of adult energy expenditure. Throughout the years, the attractive hypothesis based on this evidence has been advanced that an alteration in blood pressure regulation, as well as in thermogenesis control exerted by the sympathetic nervous system, represents the pathogenetic background for 2 diseases of common detection in current clinical practice, that is, hypertension and obesity, respectively. As far as high blood pressure is concerned, a number of studies based on indirect or direct methodologic approaches to assess neuroadrenergic function have unequivocally demonstrated that a hyperactivity of the sympathetic nervous system contributes at the development, maintenance, and progression of the hypertensive state.^1–4 They have also shown that neurogenic mechanisms favor the genesis of hypertension-related end organ damage, that is, left ventricular hypertrophy, arterial and arteriolar hypertrophy, and vascular remodelling.^5,6 Even when blood pressure is normal, an adrenergic overdrive has also been reported in the obese state,^7,8 and independent but additive increases in sympathetic activity have been described when obesity is coupled with hypertension.⁹ Traditionally, obesity-related hypertension has been regarded, at least in part, as the result of a hyperactivity of the sympathetic nervous system, related to some extent to the weight-associated increase in sympathetic cardiovascular drive.^9,10

In the present issue of the journal, Shibao et al¹¹ publish the results of an intriguing study aimed at defining . . . [Full Text of this Article]

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