Fig. 1.

Potential mechanisms of action for the anti-migraine effect of the β_1/2 receptor antagonist propranolol. By blocking β-adrenergic receptors, propranolol reduces blood pressure by decreasing sympathetic innervation [6, 7]. Furthermore, blockade of β₁-adrenergic receptors in the thalamus may block the trigeminovascular pain pathway, however, there are contradicting findings on the importance of this potential pathway. Propranolol can block capsaicin-mediated vasodilation mediated by the trigeminal nerve, possibly through agonism of presynaptic 5-HT₁ receptors [9]. Activation of 5-HT₁ receptors can block release of CGRP, leading to reduced vasodilation and nociception