title: Forearm vasoconstrictor response in uncomplicated type 1 diabetes mellitus.
abstract: BACKGROUND
  According to the 'haemodynamic hypothesis', increased tissue perfusion predisposes to microangiopathy in diabetic patients. We hypothesized that the typical haemodynamic changes underlying the increased tissue perfusion can be explained by a decreased sympathetic nerve activity caused by chronic hyperglycaemia. In this study we investigated sympathetic activity in patients with uncomplicated type 1 diabetes mellitus (DM).
  
  
  METHODS
  In 15 DM patients (DM duration 6.3 +/- 3.8 year; HbA1c 7.9 +/- 1.3%) and 16 age- and sex-matched healthy volunteers (Control), sympathetic nervous system activity was measured at rest (baseline) and during sympathoneural stimulation (lower body negative pressure (LBNP)) by means of interstitial and plasma noradrenaline (NA) sampling and power spectral analysis. Muscle sympathetic nerve activity (MSNA) was measured before (baseline) and during a cold pressure test. Forearm blood flow was measured during forearm vascular alpha- and beta-adrenergic receptor blockade.
  
  
  RESULTS
  At baseline, forearm vascular resistance (FVR), plasma NA concentrations, MSNA and heart rate variability were similar in both groups. LBNP-induced vasoconstriction was significantly attenuated in the DM group compared with the Control group (DeltaFVR: 12 +/- 4 vs. 19 +/- 3 arbitrary units, P < 0.05). The responses of plasma NA and heart rate variability did not differ.
  
  
  CONCLUSIONS
  Baseline FVR and sympathetic nerve activity are normal in patients with uncomplicated type 1 diabetes. However, the forearm vasoconstrictor response to sympathetic stimulation is attenuated, which cannot be attributed to an impaired sympathetic responsiveness.
authors.affiliation: Division of General Internal Medicine, Department of Medicine, Radboud University Nijmegen Medical Centre, the Netherlands. pvangurp@aig.umcn.nl
authors.forename: P J
authors.initials: PJ
authors.lastname: van Gurp
authors.forename: J J
authors.initials: JJ
authors.lastname: Willemsen
authors.forename: J W M
authors.initials: JW
authors.lastname: Lenders
authors.forename: H A
authors.initials: HA
authors.lastname: Ross
authors.forename: C G J
authors.initials: CG
authors.lastname: Sweep
authors.forename: P
authors.initials: P
authors.lastname: Smits
authors.forename: C J
authors.initials: CJ
authors.lastname: Tack
mesh_terms: D018674:Adrenergic Antagonists / Q000008:administration & dosage; D000328:Adult; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D003922:Diabetes Mellitus, Type 1 / Q000503:physiopathology*; D005260:Female; D005542:Forearm / Q000098:blood supply*; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D008150:Lower Body Negative Pressure; D008297:Male; D018482:Muscle, Skeletal / Q000098:blood supply; D009638:Norepinephrine / Q000032:analysis; D012039:Regional Blood Flow / Q000502:physiology*; D013564:Sympathetic Nervous System / Q000502:physiology*; D014661:Vasoconstriction / Q000187:drug effects*
chemical_list: D018674:Adrenergic Antagonists; D009638:Norepinephrine