Recently in vivo models have become available that support the pathophysiological relationship between ADMA and vascular disease, as overexpression of DDAH (which leads to a reduction of circulating ADMA concentration by about 20%) lowers systemic vascular resistance and blood pressure in mice and protects from vascular damage in various disease models, whilst genetic or pharmacological disruption of DDAH (which increases plasma ADMA levels by some 20% in mice) causes hypertension and endothelial dysfunction. This evidence concerns the gene DDAH1 and hypertensive disorder.