Asymmetric dimethylarginine [ADMA]: an emerging contributor to endothelial dysfunction in hyperthyroidism

ABSTRACT

Cardiovascular manifestations are frequent findings in patients with hyperthyroidism. Nitric oxide [NO], a key regulator of endothelial function, is synthesized from L-arginine by nitric oxide synthase [NOS]. Evidence has accumulated that asymmetric dimethylarginine [ADMA] is an endogenous competitive inhibitor of NOS. To measure plasma L-arginine and dimethylarginines [ADMA and SDMA] in patients with hyperthyroidism in order to assess their contribution to endothelial dysfunction and their relationship to plasma NO. The study was conducted on 50 newly diagnosed patients with overt hyperthyroidism as well as 30 age and sex matcned healthy controls. Plasma L-arginine, ADMA and SDMA were analyzed by HPLC. Plasma NO was measured by a colorimetric method based on Griess reagent. L-arginine, ADMA and SDMA were significantly increased, while NO and L-arginine/ADMA ratio were significantly decreased in hyperthyroid patients compared to controls. Serum freeT4 and free T3 were negatively correlated with plasma NO and L-arginine/ADMA ratio and positively correlated with L-arginine, ADMA and SDMA. Moreover, NO was significantly negatively correlated with each of the L-arginine and ADMA and significantly positively correlated with T.arginine/ADMA ratio. Results provide evidence of the presence of endothelial dysfunction in hyperthyroidism. The decrease in NO, and the increase in ADMA emphasizes that ADMA is an emerging contributor of endothelial dysfunction in hyperthyroidism