L-arginine/nitric oxide pathway activation in platelets of migraine patients with and without aura

Gallai, Virgilio; Floridi, A.; Mazzotta, Giovanni; Codini, Michela; Tognoloni, M; Vulcano, M. R.; Sartori, Marair Grácio Ferreira; Russo, Susanna; Alberti, Andrea; Michele, Flavia di; Sarchielli, Paola

doi:10.1111/j.1600-0404.1996.tb07046.x

Cited by 49 publications

(30 citation statements)

References 43 publications

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“…Gallai et al found that during attacks, higher NO 2 -and NO 3 -concentrations in platelets were seen in those with migraines as compared to the interictal period. 19 A recent study supported this finding and reported higher NO metabolite levels in platelets during migraine headaches, but not in the headache-free periods. 20 Nattero et al demonstrated higher serum NO levels during the migraine attack, but their patient group was very small (n = 7).…”

Section: Discussionmentioning

confidence: 68%

Asymmetric dimethylarginine and nitric oxide levels in migraine during the interictal period

Güldiken

Demir

Güldiken

et al. 2009

Journal of Clinical Neuroscience

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Section: Discussionmentioning

confidence: 68%

Asymmetric dimethylarginine and nitric oxide levels in migraine during the interictal period

Güldiken

Demir

Güldiken

et al. 2009

Journal of Clinical Neuroscience

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“…Our group found an increase in platelet NOS activity, both basal and collagen-stimulated, in migraine patients assessed between attacks [30]. This was accompanied by a significant rise in the intracellular messenger cyclic guanosine monophosphate (cGMP) [30].…”

Section: Platelets As a Model For The Study Of No Metabolismmentioning

confidence: 99%

“…This was accompanied by a significant rise in the intracellular messenger cyclic guanosine monophosphate (cGMP) [30]. This increase may account for some alterations in platelet function observed in migraineurs, such as the increase in platelet content of L-arginine and the reduced responsiveness to collagen; the latter finding was first shown by D'Andrea et al [5] and later confirmed by our group [4,30]. A recent study in migraine patients confirmed the activation of NOS in platelets, especially during attacks, by demonstrating increased NO end-products compared with headache-free period [31].…”

Section: Platelets As a Model For The Study Of No Metabolismmentioning

confidence: 99%

Platelets in migraine

Sarchielli

Gallai

2001

J Headache Pain

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Modification in platelet activation and aggregation has been demonstrated in migraine patients both during and between attacks. A different pattern in the secretion of platelet products has also been observed in patients affected by migraine compared with controls. The most important variation concerns a hyposecretion of dense body products. Platelets share structural and functional analogies with monoaminergic neurons, in particular serotoninergic neurons, and have been used as a peripheral model to study monaminergic function in migraine patients. A reduced turnover of serotonin has been shown in migraine patients in the interictal period, whereas a reduced content of this monoamine was detected in patients with chronic daily headache (CDH), particularly in those with analgesic abuse. Nitric oxide metabolism was also studied in platelets of migraine patients between and during attacks. An increased activity of nitric oxide synthase (NOS), which was more accentuated during attacks, was found in these patients compared to healthy individuals. The increase in platelet NOS activity was also confirmed in CDH patients in association with a reduction of serotonin content and increased calcium levels. Variations in aggregation to different agents and secretion may not, at the moment, be indicative of similar changes in cerebral circulation of migraine patients. Its occurrence should be confirmed in samples of jugular venous blood during attacks to establish a definite link with migraine pathogenesis. Moreover changes in serotonin and NO metabolism observed in platelets of migraine patients may only indirectly suggest similar modifications in the neuronal pathways involved in inducing and maintaining head pain in migraineurs.

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“…Based on these observations, our group investigated variations in ictal and interictal platelet NO production by measuring the steichiometric conversion of oxyhemoglobin to methemoglobin due to NOS activity and platelet cGMP production in migraine patients with and without aura, as compared to those of a group of age-matched control individuals [57]. Furthermore, the relationship between these variations and changes in platelet responsiveness to collagen, both ictally and interictally, were evaluated in the same patients.We found a reduced responsiveness to collagen in migraine patients, which was more accentuated during attacks.…”

Section: Cellular Modelsmentioning

confidence: 99%

Nitric oxide in primary headaches

Gallai¹,

Sarchielli²

2000

J Headache Pain

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Nitric oxide (NO) has been proposed to be a key molecule in migraine. Experimental evidence suggests its intervention in vasodilatation and activation of the trigeminovascular system as well as its involvement in the supraspinal pathways implicated in head pain processing. Other findings suggest the implication of NO in coupling neuronal and vascular changes during spreading depression. A potential role for NO has also been proposed in the pathophysiological mechanisms underlying cluster headache and chronic tension-type headache. The most relevant evidence for an increased response to exogenous NO in all primary headaches emerges from the experimental model of nitroglycerin-induced headache. Moreover, the effectiveness of non-selective NO synthase inhibitor L-N-monomethylarginine (L-NMMA) further supports the involvement of NO in migraine and chronic tension-type headache. The endogenous increase in NO production has been shown only in studies carried out during spontaneous migraine attacks which demonstrated increased levels of nitrites and cGMP in peripheral blood and internal jugular blood; the latter was followed by an increased production of algogenic and vasodilatatory prostanoids. These data suggest the potential activation of cyclooxygenase (COX) due to NO. Additional evidence suggests the increased activity of L-arginine/NO pathway in the platelet model in migraine patients. This increase was also evident between attacks, more accentuated during attacks and expressed to a greater extent during late luteal phase in menstrual migraine. Higher NO production in platelet was also demonstrated in patients affected by chronic daily headache and they are accompanied by significant lower serotonin content and higher levels of intracellular calcium. Whether these changes may be expressed in the central nervous system is a matter of discussion. These data taken together suggest a crucial role played by NO in neurovascular headaches and chronic headaches. Further research concerning NO in all primary headaches will be aimed at verifying changes of reliable markers of NO metabolism and NO effects, to better understand the complex COX/NO synthase (NOS) interactions, to investigate the effectiveness of selective NOS inhibitors in discriminating neural versus vascular involvement of NO.

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L-arginine/nitric oxide pathway activation in platelets of migraine patients with and without aura

Cited by 49 publications

References 43 publications

Asymmetric dimethylarginine and nitric oxide levels in migraine during the interictal period

Asymmetric dimethylarginine and nitric oxide levels in migraine during the interictal period

Platelets in migraine

Nitric oxide in primary headaches

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