RaffaeleNapoli, Dept. of Internal Medicine, University Federico II, Via pansini, 5 - 80131 ,Naples, Italynapoli@unina.it
L. Saccà
Submitted September 02, 2009
We thank Dr. Devor for his interest in our article on vascular reactivity in patients with migraine. [1] Endothelial dysfunction and abnormal vascular reactivity are involved in the onset and progression of atherosclerosis and subsequently the increased risk of cardiovascular diseases.
Given the increased risk of cardiovascular events associated with migraine, we aimed to explore the reactivity of both endothelial and vascular smooth muscle cells (VSMCs) in patients with migraine in the headache-free state. We found that in migraine patients studied in the interictal period, endothelial function is normal and a clear defect in the VSMCs response emerges. In human vessels, acetylcholine vasodilatory response is due to the stimulation of specific receptors located on the surface of the endothelial cells which in turn activate nitric oxide synthase in order to produce nitric oxide (NO).
Once released, NO triggers vasodilation by stimulating cGMP production in the VSMCs. In our data, the response to the intra-arterial infusion of acetylcholine is reduced in patients with migraine. However, this reduction is not due to a defect in the ability of acetylcholine to induce NO production and release by the endothelial cells, but rather to a severe impairment of VSMCs to respond to NO stimulation. This is demonstrated because we detected a normal release of NO during acetylcholine infusion by the endothelial cells. In addition, there was an impaired vasodilation during the infusion of sodium nitroprusside (a NO donors) in patients with migraine due to the insufficient response to NO by the VSMCs.
Therefore, acetylcholine response by the endothelial cells in patients with migraine during the interictal period is normal. Since we were interested in the mechanisms of cardiovascular risk, we also studied vascular reactivity in the brachial artery as a well established model of coronary vascular reactivity. However, the relationship between peripheral vascular reactivity and cerebral circulation is still unclear.
Since we studied vascular reactivity in the headache-free period, the vascular mechanisms underlying the migraine attack in both peripheral and cerebral circulation cannot be clarified by our study. The possibility arises that vascular reactivity can be different during the migraine attack.
Disclosure: Drs. Napoli and Saccà received compensation for a study from Pfizer Italia.
We thank Dr. Devor for his interest in our article on vascular reactivity in patients with migraine. [1] Endothelial dysfunction and abnormal vascular reactivity are involved in the onset and progression of atherosclerosis and subsequently the increased risk of cardiovascular diseases.
Given the increased risk of cardiovascular events associated with migraine, we aimed to explore the reactivity of both endothelial and vascular smooth muscle cells (VSMCs) in patients with migraine in the headache-free state. We found that in migraine patients studied in the interictal period, endothelial function is normal and a clear defect in the VSMCs response emerges. In human vessels, acetylcholine vasodilatory response is due to the stimulation of specific receptors located on the surface of the endothelial cells which in turn activate nitric oxide synthase in order to produce nitric oxide (NO).
Once released, NO triggers vasodilation by stimulating cGMP production in the VSMCs. In our data, the response to the intra-arterial infusion of acetylcholine is reduced in patients with migraine. However, this reduction is not due to a defect in the ability of acetylcholine to induce NO production and release by the endothelial cells, but rather to a severe impairment of VSMCs to respond to NO stimulation. This is demonstrated because we detected a normal release of NO during acetylcholine infusion by the endothelial cells. In addition, there was an impaired vasodilation during the infusion of sodium nitroprusside (a NO donors) in patients with migraine due to the insufficient response to NO by the VSMCs.
Therefore, acetylcholine response by the endothelial cells in patients with migraine during the interictal period is normal. Since we were interested in the mechanisms of cardiovascular risk, we also studied vascular reactivity in the brachial artery as a well established model of coronary vascular reactivity. However, the relationship between peripheral vascular reactivity and cerebral circulation is still unclear.
Since we studied vascular reactivity in the headache-free period, the vascular mechanisms underlying the migraine attack in both peripheral and cerebral circulation cannot be clarified by our study. The possibility arises that vascular reactivity can be different during the migraine attack.
Disclosure: Drs. Napoli and Saccà received compensation for a study from Pfizer Italia.