Nitric oxide in blood vessels

An artery is not a rigid tube: it opens and closes, and much of that control comes from inside the artery itself. The layer that lines it on the inside, the endothelium, makes its own vasodilator, that is, its own substance for opening the artery. That substance is called endothelium-derived relaxing factor, and it acts as nitric oxide.

It is made by an enzyme called endothelial nitric oxide synthase, from an amino acid, L-arginine. Once made, it leaves the cell: it diffuses toward the outer layer and there it attaches to another enzyme, guanylate cyclase, which lives in the smooth muscle that wraps around the vessel. It is a message that the inner wall sends to the muscle outside.

What follows is a short chain of events. That enzyme turns GTP into cyclic GMP, an internal messenger that activates certain kinases, and that pathway ends up sequestering the cell's calcium. And with no calcium available the muscle relaxes and the vessel widens.

Nitric oxide does one more thing: it curbs platelet adhesion, which is the ability of platelets to stick in place. That is why, when it runs low, endothelial dysfunction can appear, which is an early step in atherosclerosis, the hardening and narrowing of the arteries.