ReviewsThe sympathetic nervous system and the metabolic syndromeMancia, Giuseppea; Bousquet, Pascalb; Elghozi, Jean Lucc; Esler, Murrayd; Grassi, Guidoa; Julius, Stevoe; Reid, Johnf; Van Zwieten, Peter AgAuthor Information aOspedale San Gerardo dei Tintori, Università Milano-Bicocca, Monza (Milan), Italy bULP – Faculté de Médecine, Strasbourg, France cHôpital Necker Enfants Malades, UF de Pharmacologie Clinique, Paris, France dBaker Medical Research Institute, Melbourne, Australia eThe University of Michigan Health System, Department of Internal Medicine, Ann Arbor, Michigan, USA fUniversity of Glasgow, Department of Medicine and Therapeutics, Gardiner Institute, Glasgow, Scotland gAcademic Medical Center University of Amsterdam, Departments of Pharmacotherapy, Cardiology and Cardiopulmonary Surgery, Amsterdam, The Netherlands Received 22 June, 2006 Revised 13 November, 2006 Accepted 14 December, 2006 Correspondence and requests for reprints to Giuseppe Mancia, Clinica Medica, Ospedale San Gerardo dei Tintori, Via Pergolesi 33, 20052 Monza (Milan), Italy Tel: +39 039 233 374; fax: +39 039 322 274; e-mail: [email protected] Journal of Hypertension: May 2007 - Volume 25 - Issue 5 - p 909-920 doi: 10.1097/HJH.0b013e328048d004 Buy Metrics Abstract Studies performed in the past two decades have unequivocally shown that several of the components of the metabolic syndrome are associated with indirect and direct markers of adrenergic overdrive. This is the case for hypertension and obesity, in which resting tachycardia, elevated plasma norepinephrine values, increased sympathetic nerve traffic, as well as augmented levels of total and regional norepinephrine spillover have been reported. This is also the case for insulin resistance, i.e. a metabolic condition frequently complicating the various components of the pathological condition identified as the ‘metabolic syndrome’. After briefly describing the epidemiological and the cardiovascular risk profile of the disease, this paper will examine the behaviour of the sympathetic nervous system in the metabolic syndrome as well as the mechanisms potentially responsible for this neurogenic abnormality. This will be followed by an analysis of the role played by neuroadrenergic factors in disease progression as well as in the pathogenesis of its complications. Finally, the therapeutic implications of these findings will be highlighted. © 2007 Lippincott Williams & Wilkins, Inc.