Arterial hypertension: oxidative stress and endothelial disfunction

Abstract

The aim of the study was to investigate the pathogenetic significance of oxidative stress (OS) in the development of endothelial vascular dysfunction (ED) in essential arterial hypertension (AH) and to determine the possibilities of the markers usage for evaluation of antihypertensive drugs influence on leukocyte-endothelial interaction (LEI). Methods of research included evaluation of OS - oxidative metabolism of polymorphonuclear leukocytes (PML) by chemiluminescence (ChL), proinflammatory cytokines (interleukin-1/spl beta/, TNF-/spl alpha/) by immunoenzyme methods, and ED, including evaluation of nitric oxide (NO) and hemostasis procoagulant factors. Increase in OS and ED in AH were revealed. In the frames of 4-week randomized controlled clinical trial AT II receptors antagonist valsartan and ACE inhibitor perindopril, contrary to beta-adrenergic blocking agent atenolol, except achievement of target arterial pressure, normalize or considerably lower the raised oxidative stress and endothelial dysfunction, including proinflammatory cytokines and procoagulant factors activity, at arterial hypertension of 2-3 severity degrees with further delay of pathological process progressing in patients. This investigation proves that the OS has important pathogenetic value for ED development at AH when arising damages of LEI conduct to proinflammation, vasoconstriction, prothrombosis, vascular remodeling and to defeat organs-targets.