Skip to main content
. Author manuscript; available in PMC: 2020 Aug 25.
Published in final edited form as: Atherosclerosis. 2019 Nov 14;292:201–203. doi: 10.1016/j.atherosclerosis.2019.11.001

Fig. 1.

Fig. 1.

The opposite effects of NO and ET-1 on vascular function are counterbalanced in healthy tissue and dysregulated in atherosclerosis.

A new mechanism of regulation is the ability of ET-1 in vascular endothelial cells and macrophages to induce arginase expression, which then competes for l-arginine substrate with NO synthase, thereby reducing NO bioavailability.