Evidence from human models of migraine as well as other lines of research suggest a putative model for the genesis of migraine attacks.1 Within vascular smooth muscle cells of cephalic arteries, migraine-inducing substances act through intracellular second messengers including cyclic adenosine monophosphate (cAMP) or cyclic guanosine monophosphate (cGMP) to eventually cause the opening of ATP-sensitive potassium (KATP) channels or large-conductance Ca2+-activated K+ (BKCa) channels. This release of potassium from vascular smooth muscle cells and subsequently vasodilation. The efflux of potassium might activate adjacent perivascular nerve fibers to trigger the perception of migraine pain.
AMP = Adenosine Monophosphate; ATP = Adenosine Triphosphate; CGRP = Calcitonin Gene-Related Peptide; GMP = Guanosine Monophosphate; GTP = Guanosine Triphosphate; NO = Nitric Oxide; PACAP-38 = Pituitary Adenylate Activating Polypeptide-38; PDE-3; Phosphodiesterase-3; PDE-5; Phosphodiesterase-5; PKA = Protein Kinase A; PKG = Protein Kinase G.
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