ADMA interferes with L-arginine in the production of nitric oxide (NO), a key chemical involved in normal endothelial function and, by extension, cardiovascular health.

Patrick Vallance and his London co-workers first noted the interference role for asymmetric dimethylarginine in the early 1990s.

[3] Thus a spiralling effect occurs with high endothelial LDL levels causing greater ADMA values, which in turn inhibit NO production needed to promote vasodilation.

The elimination of ADMA occurs through urine excretion and metabolism by the enzyme dimethylarginine dimethylaminohydrolase (DDAH).

[12][13] The hope is that such intervention might not only improve endothelial function but also reduce clinical symptoms of overt cardiovascular disease.

Elevated levels of ADMA seems to modify this effect and so may have consequences for patients' responsiveness to taking statins.