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Endothelial Dysfunction
Certain vasodilators exert their effects by working via the endothelium, specifically by enhancing the production of nitric oxide from endothelial nitric oxide synthase. Normally, nitric oxide then works to promote vasodilation in a blood vessel through its own mechanisms, preventing the release of agents that promote vasoconstriction. Endothelial dysfunction leading to a deficiency in nitric oxide has been found to be associated with coronary vasospasm in some cases. Vasodilatory agents with mechanisms that are dependent on a functional endothelial nitric oxide synthase can cause vasoconstriction instead in the setting of endothelial dysfunction, promoting coronary vasospasm. This is also supported by the fact that vasospastic angina is responsive to nitrate, a vasodilator with a mechanism independent of a functional endothelium.

Chronic Inflammation
Markers of low grade chronic inflammation have been found in cases of coronary vasospasm.

When large coronary arteries undergo vasospasm, this can lead to either complete or transient occlusion of blood flow within the artery. As a result, ischemia to the tissues served by the artery can occur.