Key result
Lomerizine strongly inhibits serotonin-induced vasoconstriction and calcium release, suggesting 5-HT2A receptor antagonism.
Why the study?
The mechanisms by which lomerizine inhibits serotonin-induced contraction of the basilar artery compared to nifedipine were unclear.
Does lomerizine inhibit serotonin-induced contraction of the basilar artery in a preclinical model?
Does lomerizine inhibit serotonin-induced contraction of the basilar artery in a preclinical model?
Lomerizine may ameliorate basilar-type migraines by preventing 5-HT-induced contraction in the basilar artery via antagonistic effects against both voltage-dependent Ca2+ channels and 5-HT2A receptors.
Answers are grounded in this paper and cite their sources.
Does not support clinical use; leaves open lomerizine as 5-HT2A antagonist for cerebrovascular research.
We examined the effects of lomerizine on serotonin (5-hydroxytryptamine, 5-HT)-induced contraction of the basilar artery and compared them with those of nifedipine. Although both lomerizine and nifedipine completely blocked K(+)-induced vasoconstriction, 5-HT-induced vasoconstriction was more strongly inhibited by lomerizine than nifedipine. A 5-HT(2A) antagonist inhibited the 5-HT-induced vasoconstriction, but a 5-HT(1B) antagonist did not. Lomerizine, but not nifedipine, suppressed 5-HT-induced Ca(2+) release in 5-HT(2A)-expressing HEK293 cells. Moreover, neither antagonist affected ATP-induced Ca(2+) release. These results suggest that lomerizine may inhibit not only voltage-dependent Ca(2+) channels but also 5-HT(2A) receptors and so inhibit 5-HT-induced contraction in the basilar artery.
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Ishii et al. (2009) studied Migraine. Lomerizine vs. Nifedipine, Verapamil, or Control was evaluated on Inhibition of 5-HT-induced contraction of the basilar artery and Ca2+ release (p=<0.05). Lomerizine strongly inhibited serotonin-induced vasoconstriction in the rat basilar artery and suppressed serotonin-induced calcium release, suggesting it acts as a 5-HT2A receptor antagonist.
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