Endothelial dysfunction and ADMA in pathogenesis of arterial hypertension

Abstract

Cardiovascular diseases (CVD) are today one of the major healthcare problems of the world population. Endothelial dysfunction (ED) reflects prominent abnormalities observed in these disorders. Nitric oxide is one of the most potent endothelial vasodilators and has also anti-inflammatory and antithrombotic properties. NO-mediated endothelium - dependent vasodilatation plays a crucial role in regulation of vascular tone. Impaired activity of NO-dependent metabolic pathways in endothelium may increase the risk of CVD and may be an important pathophysiological link leading to development of arterial hypertension (HTA). Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of NO synthase, which may cause ED due to decreased NO-availability. ADMA may be not only a marker, but also an active mediator in pathogenesis of CVD. Its levels have been shown to be elevated in variety of disorders, e.g. in hypertension. This article gives a brief review of contemporary state of knowledge regarding ED, ADMA and HTA. Pathophysiology of ED and HTA and possible pharmacological interventions aiming the modulation of ADMA level are discussed.