title: Vascular smooth muscle cell dysfunction in patients with migraine.
abstract: BACKGROUND
  Migraine is associated with increased risk of cardiovascular disease, but the mechanisms are unclear.
  
  
  OBJECTIVE
  To investigate the activity of endothelial and vascular smooth muscle cells (VSMCs) in patients with migraine.
  
  
  METHODS
  Case-control study of 12 patients with migraine without aura and 12 matched healthy control subjects. Endothelial and VSMC components of vascular reactivity were explored by plethysmography measurement of forearm blood flow (FBF) during infusions of vasoactive agents into the brachial artery. Forearm production of nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) was also quantified.
  
  
  RESULTS
  In patients with migraine, the vasodilating effect of acetylcholine (ACh), an endothelium-dependent vasodilator, was markedly reduced (p < 0.001 by analysis of variance). In response to the highest dose of ACh, FBF rose to 8.6 +/- 2.2 in patients with migraine and to 22.7 +/- 3.0 mL x dL(-1) x min(-1) in controls (p = 0.001). The dose-response curve to nitroprusside, a vasodilator directly acting on VSMCs, was depressed in patients with migraine (p < 0.001 by analysis of variance). The maximal response of FBF to nitroprusside was 12.1 +/- 2.0 in patients with migraine and 24.1 +/- 1.8 mL x dl(-1) x min(-1) in controls (p < 0.001). During ACh infusion, NO release from the endothelium was similar in patients and controls. In contrast, there was a marked release of cGMP from VSMCs in controls, but not in patients with migraine (-1.9 +/- 2.2 in patients with migraine and -19.1 +/- 5.4 nmol x dL(-1) x min(-1) in controls; p = 0.03).
  
  
  CONCLUSIONS
  Patients with migraine are characterized by a distinct vascular smooth muscle cell dysfunction, revealed by impaired cyclic guanosine monophosphate and hemodynamic response to nitric oxide.
authors.affiliation: Department of Internal Medicine, University Federico II School of Medicine, Naples, Italy. napoli@unina.it
authors.forename: R
authors.initials: R
authors.lastname: Napoli
authors.forename: V
authors.initials: V
authors.lastname: Guardasole
authors.forename: E
authors.initials: E
authors.lastname: Zarra
authors.forename: M
authors.initials: M
authors.lastname: Matarazzo
authors.forename: C
authors.initials: C
authors.lastname: D'Anna
authors.forename: F
authors.initials: F
authors.lastname: Saccà
authors.forename: F
authors.initials: F
authors.lastname: Affuso
authors.forename: A
authors.initials: A
authors.lastname: Cittadini
authors.forename: P B
authors.initials: PB
authors.lastname: Carrieri
authors.forename: L
authors.initials: L
authors.lastname: Saccà
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000328:Adult; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001916:Brachial Artery / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D002318:Cardiovascular Diseases / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology*; D016022:Case-Control Studies; D015897:Comorbidity; D006152:Cyclic GMP / Q000378:metabolism; D042783:Endothelial Cells / Q000187:drug effects / Q000378:metabolism; D005260:Female; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D006801:Humans; D008297:Male; D008881:Migraine Disorders / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism* / Q000503:physiopathology*; D009569:Nitric Oxide / Q000378:metabolism; D009599:Nitroprusside / Q000494:pharmacology; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D014665:Vasodilator Agents; D009599:Nitroprusside; D009569:Nitric Oxide; D006152:Cyclic GMP; D000109:Acetylcholine