Department of Neurology, Danish Headache Center, Denmark.
Cephalalgia. 2010 Nov;30(11):1346-53. doi: 10.1177/0333102410363491. Epub 2010 Apr 7.
There is a striking similarity between the migraine-provoking effect of the nitric oxide (NO) donor glyceryl trinitrate (GTN) and that of calcitonin gene-related peptide (CGRP). We tested the hypothesis that NO releases CGRP to cause the delayed migraine attack after GTN.
In a double-blind-cross-over study, 13 migraine without aura (MO) patients were administered GTN 0.5 µg/kg/minute for 20 minutes and subsequently BIBN4096BS (olcegepant) 10 mg or placebo. Headache scores and development of MO were followed for 24 hours.
MO developed in seven of 13 with olcegepant and in nine of 13 with placebo (p=0.68). The headache scores were similar after the two treatments (p=0.58). Thus CGRP receptor blockade did not prevent GTN-induced migraine.
The present study indicates that NO does not induce migraine by liberating CGRP. The most likely explanation for our findings is that CGRP has its effect higher than NO in the cascade of events leading to MO attacks.
一氧化氮（NO）供体硝化甘油（GTN）引起偏头痛的作用与降钙素基因相关肽（CGRP）非常相似。我们检验了这样一个假设，即 NO 释放 CGRP 引起 GTN 后延迟的偏头痛发作。
在一项双盲交叉研究中，13 名无先兆偏头痛（MO）患者接受 GTN 0.5μg/kg/min 输注 20 分钟，随后给予 BIBN4096BS（olcegepant）10mg 或安慰剂。在 24 小时内监测头痛评分和 MO 的发生情况。
13 名患者中有 7 名在服用 olcegepant 后发生 MO，13 名患者中有 9 名在服用安慰剂后发生 MO（p=0.68）。两种治疗后头痛评分相似（p=0.58）。因此，CGRP 受体阻断剂不能预防 GTN 诱导的偏头痛。
本研究表明，NO 通过释放 CGRP 不会引起偏头痛。我们研究结果最可能的解释是，在导致 MO 发作的级联反应中，CGRP 的作用高于 NO。
