RT Journal Article
SR Electronic
T1 Vascular smooth muscle cell dysfunction in patients with migraine
JF Neurology
JO Neurology
FD Lippincott Williams & Wilkins
SP 2111
OP 2114
DO 10.1212/WNL.0b013e3181aa53ce
VO 72
IS 24
A1 Napoli, R.
A1 Guardasole, V.
A1 Zarra, E.
A1 Matarazzo, M.
A1 D'Anna, C.
A1 Saccà, F.
A1 Affuso, F.
A1 Cittadini, A.
A1 Carrieri, P. B.
A1 Saccà, L.
YR 2009
UL http://n.neurology.org/content/72/24/2111.abstract
AB 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 × dL−1 × 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 × dl−1 × 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 × dL−1 × 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. ACh=acetylcholine; ADMA=asymmetric dimethylarginine; BMI=body mass index; cGMP=cyclic guanosine monophosphate; DBP=diastolic blood pressure; FBF=forearm blood flow; HR=heart rate; NO=nitric oxide; NP=nitroprusside; SBP=systolic blood pressure; VSMC=vascular smooth muscle cell.