Nitroglycerin-induced headache is not dependent on histamine release: support for a direct nociceptive action of nitric oxide
Research output: Contribution to journal › Journal article › Research › peer-review
Standard
Nitroglycerin-induced headache is not dependent on histamine release : support for a direct nociceptive action of nitric oxide. / Iversen, Helle Klingenberg; Olesen, J.
In: Cephalalgia : an international journal of headache, Vol. 14, No. 6, 12.1994, p. 437-42.Research output: Contribution to journal › Journal article › Research › peer-review
Harvard
APA
Vancouver
Author
Bibtex
}
RIS
TY - JOUR
T1 - Nitroglycerin-induced headache is not dependent on histamine release
T2 - support for a direct nociceptive action of nitric oxide
AU - Iversen, Helle Klingenberg
AU - Olesen, J
PY - 1994/12
Y1 - 1994/12
N2 - The molecular mechanisms of migraine pain have not yet been clarified. Monoamine and the peptide neurotransmitters involved in neurogenic inflammation do not cause significant head pain. Our previous studies of glyceryl trinitrate (GTN) and histamine-induced headaches have suggested that nitric oxide (NO) is the causative molecule in migraine pain. We furthermore suggest that substances capable of inducing experimental vascular headache do so via a common mediator which is NO. Finally, it is suggested that drugs exert their antimigraine activity by inhibiting NO or subsequent steps in the cascade of intracellular reactions triggered by NO. These novel observations change current views on vascular headache mechanisms and the importance of NO as an initiator of the migraine attacks dictates new approaches to the pharmacological treatment of migraine and other vascular headaches.
AB - The molecular mechanisms of migraine pain have not yet been clarified. Monoamine and the peptide neurotransmitters involved in neurogenic inflammation do not cause significant head pain. Our previous studies of glyceryl trinitrate (GTN) and histamine-induced headaches have suggested that nitric oxide (NO) is the causative molecule in migraine pain. We furthermore suggest that substances capable of inducing experimental vascular headache do so via a common mediator which is NO. Finally, it is suggested that drugs exert their antimigraine activity by inhibiting NO or subsequent steps in the cascade of intracellular reactions triggered by NO. These novel observations change current views on vascular headache mechanisms and the importance of NO as an initiator of the migraine attacks dictates new approaches to the pharmacological treatment of migraine and other vascular headaches.
KW - Analysis of Variance
KW - Cross-Over Studies
KW - Double-Blind Method
KW - Headache
KW - Hemodynamics
KW - Histamine Release
KW - Humans
KW - Nitric Oxide
KW - Nitroglycerin
KW - Pain
KW - Radial Artery
KW - Reproducibility of Results
KW - Temporal Arteries
M3 - Journal article
C2 - 7535192
VL - 14
SP - 437
EP - 442
JO - Cephalalgia
JF - Cephalalgia
SN - 0800-1952
IS - 6
ER -
ID: 128984215