Triptans (e.g., sumatriptan) abort acute migraine by a dual mechanism. The two primary mechanisms are:

• A 5-HT2A receptor antagonism blocking cortical spreading depression
• B 5-HT3 receptor antagonism reducing nausea and vomiting
• C D2 receptor agonism in mesolimbic pathways reducing pain perception
• D 5-HT1B receptor agonism (cranial vasoconstriction) and 5-HT1D receptor agonism (inhibiting trigeminal neuropeptide release) ✓

Explanation

Triptans are selective 5-HT1B/1D receptor agonists. 5-HT1B agonism constricts dilated cranial blood vessels (meningeal arteries), reducing pulsatile distension that activates perivascular trigeminovascular nerve endings. 5-HT1D agonism on presynaptic trigeminal nerve terminals inhibits release of CGRP, substance P, and other vasoactive neuropeptides, blocking neurogenic inflammation in the meninges. These two complementary mechanisms make triptans specific anti-migraine agents without general analgesic properties.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

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Written and medically reviewed by the StethoPrep medical team.