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Fig. 2 | The Journal of Headache and Pain

Fig. 2

From: Provoked versus spontaneous migraine attacks: pathophysiological similarities and differences

Fig. 2

cGMP-dependent pathways in migraine pathophysiology. In vascular smooth muscle cells of the intracranial arteries, nitric oxide (NO) from glyceryl trinitrate (GTN) increases levels of cyclic guanosine monophosphate (cGMP). This activates the cGMP-dependent protein kinase (protein kinase G) which increases opening of adenosine triphosphate-sensitive potassium (KATP) channels and large conductance calcium-activated potassium (BKCa) channels. It will similar to the cAMP-dependent pathway ultimately activate and sensitize perivascular trigeminal afferents (see Fig. 1) [2]. BKCA, large conductance calcium-activated potassium channels; cGMP, cyclic guanosine monophosphate; GTN, glyceryl trinitrate; GTP, guanosine triphosphate; KATP-channels, adenosine triphosphate-sensitive potassium channels; NO, nitric oxide; Protein kinase G, cGMP-dependent protein kinase; sGC, soluble guanylate cyclase

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