The ADMA/Angiotensin II pathway in endothelial dysfunction

The asymmetric dimethylarginin (ADMA) is currently an endogenous structural analogue of L-arginine, is so involved in inducing vascular diseases associated with a number of risk factors such as hypercholesterolemia, hypertension, diabetes, cancer and cigarette smoking. ADMA in animal models and in humans causes endothelial disfunction.Physiological concentrations of ADMA in the presence of Ang II, Losartan, PD123319 and Apocynin do not increase superoxide production but also in terms of damage tend to maintain stable hypothermic this production. Instead HUVECs treated with ADMA [10-4 M] show an not significant increase? in comparison with controls. Testing the effect of increasing concentrations of ADMA without hypothermia treatment on HUVEC peroxide synthesis are inversely proportional. dysfunction and its infusion causes vasoconstrictive effects and arteriolar resistance increase especially in humans[196]. In the process of endothelial dysfunction many factors are involved including a leading role in the action of the radical species (ROS and RNS), in the time. The aim of this work is to assess the effect of different concentrations of ADMA on human endothelial umbillical vein cells in cellular physiological and patho-physiological conditions in the presence of Angiontensin II