EDN1 and atherosclerosis: However, pathological stimuli reduced eNOS levels in ECs and promoted production of the vasoconstrictor ET-1 (endothelin-1), PAI-1 (plasminogen activator inhibitor-1) and transcription regulator HIF-1 (hypoxia-inducible factor 1), thus increasing platelet aggregation, endothelial procoagulant effect and smooth muscle cell proliferation and migration, which, in total, resulted in increased risk of thrombosis and atherosclerosis [29].