Nitric oxide-related drug targets in headache

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Nitric oxide-related drug targets in headache. / Olesen, Jes.

I: Neurotherapeutics, Bind 7, Nr. 2, 01.04.2010, s. 183-90.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Olesen, J 2010, 'Nitric oxide-related drug targets in headache', Neurotherapeutics, bind 7, nr. 2, s. 183-90. https://doi.org/10.1016/j.nurt.2010.03.006

APA

Olesen, J. (2010). Nitric oxide-related drug targets in headache. Neurotherapeutics, 7(2), 183-90. https://doi.org/10.1016/j.nurt.2010.03.006

Vancouver

Olesen J. Nitric oxide-related drug targets in headache. Neurotherapeutics. 2010 apr. 1;7(2):183-90. https://doi.org/10.1016/j.nurt.2010.03.006

Author

Olesen, Jes. / Nitric oxide-related drug targets in headache. I: Neurotherapeutics. 2010 ; Bind 7, Nr. 2. s. 183-90.

Bibtex

@article{96652316002741b08005debaa0fffafd,
title = "Nitric oxide-related drug targets in headache",
abstract = "SUMMARY: Nitric oxide (NO) is a very important molecule in the regulation of cerebral and extra cerebral cranial blood flow and arterial diameters. It is also involved in nociceptive processing. Glyceryl trinitrate (GTN), a pro-drug for NO, causes headache in normal volunteers and a so-called delayed headache that fulfils criteria for migraine without aura in migraine sufferers. Blockade of nitric oxide synthases (NOS) by L-nitromonomethylarginine effectively treats attacks of migraine without aura. Similar results have been obtained for chronic the tension-type headache and cluster headache. Inhibition of the breakdown of cyclic guanylate phosphate (cGMP) also provokes migraine in sufferers, indicating that cGMP is the effector of NO-induced migraine. Similar evidence suggests an important role of NO in the tension-type headache and cluster headache. These very strong data from human experimentation make it highly likely that antagonizing NO effects will be effective in the treatment of primary headaches. Nonselective NOS inhibitors are likely to have side effects whereas selective compounds are now in early clinical trials. Antagonizing the rate limiting cofactor tetrahydrobiopterin seems another very likely new treatment. It is more unlikely that antagonism of cGMP or its formation will be feasible, but augmenting its breakdown via phosphodiesterase activation is a possibility, as well as other ways of inhibiting the NO-cGMP pathway.",
author = "Jes Olesen",
note = "Copyright 2010 The American Society for Experimental NeuroTherapeutics, Inc. Published by Elsevier Inc. All rights reserved.",
year = "2010",
month = apr,
day = "1",
doi = "http://dx.doi.org/10.1016/j.nurt.2010.03.006",
language = "English",
volume = "7",
pages = "183--90",
journal = "Neurotherapeutics",
issn = "1933-7213",
publisher = "Springer",
number = "2",

}

RIS

TY - JOUR

T1 - Nitric oxide-related drug targets in headache

AU - Olesen, Jes

N1 - Copyright 2010 The American Society for Experimental NeuroTherapeutics, Inc. Published by Elsevier Inc. All rights reserved.

PY - 2010/4/1

Y1 - 2010/4/1

N2 - SUMMARY: Nitric oxide (NO) is a very important molecule in the regulation of cerebral and extra cerebral cranial blood flow and arterial diameters. It is also involved in nociceptive processing. Glyceryl trinitrate (GTN), a pro-drug for NO, causes headache in normal volunteers and a so-called delayed headache that fulfils criteria for migraine without aura in migraine sufferers. Blockade of nitric oxide synthases (NOS) by L-nitromonomethylarginine effectively treats attacks of migraine without aura. Similar results have been obtained for chronic the tension-type headache and cluster headache. Inhibition of the breakdown of cyclic guanylate phosphate (cGMP) also provokes migraine in sufferers, indicating that cGMP is the effector of NO-induced migraine. Similar evidence suggests an important role of NO in the tension-type headache and cluster headache. These very strong data from human experimentation make it highly likely that antagonizing NO effects will be effective in the treatment of primary headaches. Nonselective NOS inhibitors are likely to have side effects whereas selective compounds are now in early clinical trials. Antagonizing the rate limiting cofactor tetrahydrobiopterin seems another very likely new treatment. It is more unlikely that antagonism of cGMP or its formation will be feasible, but augmenting its breakdown via phosphodiesterase activation is a possibility, as well as other ways of inhibiting the NO-cGMP pathway.

AB - SUMMARY: Nitric oxide (NO) is a very important molecule in the regulation of cerebral and extra cerebral cranial blood flow and arterial diameters. It is also involved in nociceptive processing. Glyceryl trinitrate (GTN), a pro-drug for NO, causes headache in normal volunteers and a so-called delayed headache that fulfils criteria for migraine without aura in migraine sufferers. Blockade of nitric oxide synthases (NOS) by L-nitromonomethylarginine effectively treats attacks of migraine without aura. Similar results have been obtained for chronic the tension-type headache and cluster headache. Inhibition of the breakdown of cyclic guanylate phosphate (cGMP) also provokes migraine in sufferers, indicating that cGMP is the effector of NO-induced migraine. Similar evidence suggests an important role of NO in the tension-type headache and cluster headache. These very strong data from human experimentation make it highly likely that antagonizing NO effects will be effective in the treatment of primary headaches. Nonselective NOS inhibitors are likely to have side effects whereas selective compounds are now in early clinical trials. Antagonizing the rate limiting cofactor tetrahydrobiopterin seems another very likely new treatment. It is more unlikely that antagonism of cGMP or its formation will be feasible, but augmenting its breakdown via phosphodiesterase activation is a possibility, as well as other ways of inhibiting the NO-cGMP pathway.

U2 - http://dx.doi.org/10.1016/j.nurt.2010.03.006

DO - http://dx.doi.org/10.1016/j.nurt.2010.03.006

M3 - Journal article

VL - 7

SP - 183

EP - 190

JO - Neurotherapeutics

JF - Neurotherapeutics

SN - 1933-7213

IS - 2

ER -

ID: 34126569