title: Neuroadrenergic and reflex abnormalities in patients with metabolic syndrome.
abstract: OBJECTIVE
  Previous studies have shown that alterations in vascular, metabolic, inflammatory and haemocoagulative functions characterise the metabolic syndrome. Whether this is also the case for sympathetic function is not clear. We therefore aimed to clarify this issue and to determine whether metabolic or reflex mechanisms might be responsible for the possible adrenergic dysfunction.
  
  
  METHODS
  In 43 healthy control subjects (age 48.2+/-1.0 years, mean+/-SEM) and in 48 untreated age-matched subjects with metabolic syndrome (National Cholesterol Education Program's Adult Treatment Panel III Report criteria) we measured, along with anthropometric and metabolic variables, blood pressure (Finapres), heart rate (ECG) and efferent postganglionic muscle sympathetic nerve activity (microneurography) at rest and during baroreceptor manipulation (vasoactive drug infusion technique).
  
  
  RESULTS
  Compared with control subjects, subjects with metabolic syndrome had higher BMI, waist circumference, blood pressure, cholesterol, triglycerides, insulin and homeostasis model assessment (HOMA) index values but lower HDL cholesterol values. Sympathetic nerve traffic was significantly greater in subjects with metabolic syndrome than in control subjects (61.1+/-2.6 vs 43.8+/-2.8 bursts/100 heartbeats, p<0.01), the presence of sympathetic activation also being detectable when the metabolic syndrome did not include hypertension as a component. Muscle sympathetic nerve traffic correlated directly and significantly with waist circumference (r=0.46, p<0.001) and HOMA index (r=0.49, p<0.001) and was inversely related to baroreflex sensitivity (r=-0.44, p<0.001), which was impaired in the metabolic syndrome.
  
  
  CONCLUSIONS
  These data provide evidence that the metabolic syndrome is characterised by sympathetic activation and that this abnormality (1) is also detectable when blood pressure is normal and (2) depends on insulin resistance as well as on reflex alterations.
authors.affiliation: Department of Internal Medicine, Prevention and Medicine Biotechnologies, University Milano-Bicocca, Milan, Italy.
authors.forename: G
authors.initials: G
authors.lastname: Grassi
authors.forename: R
authors.initials: R
authors.lastname: Dell'Oro
authors.forename: F
authors.initials: F
authors.lastname: Quarti-Trevano
authors.forename: F
authors.initials: F
authors.lastname: Scopelliti
authors.forename: G
authors.initials: G
authors.lastname: Seravalle
authors.forename: F
authors.initials: F
authors.lastname: Paleari
authors.forename: P L
authors.initials: PL
authors.lastname: Gamba
authors.forename: G
authors.initials: G
authors.lastname: Mancia
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure; D004837:Epinephrine / Q000097:blood; D005260:Female; D006339:Heart Rate; D006706:Homeostasis; D006801:Humans; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood / Q000503:physiopathology*; D008875:Middle Aged; D009638:Norepinephrine / Q000097:blood; D012016:Reference Values; D012018:Reflex / Q000502:physiology*; D013564:Sympathetic Nervous System / Q000503:physiopathology*
chemical_list: D001786:Blood Glucose; D009638:Norepinephrine; D004837:Epinephrine