The effect of valsartan and nebivolol treatment on ADMA and pentraxin-3 levels in hypertensive patients

Abstract

Long pentraxin 3 (PTX3) is a recently discovered multimeric inflammatory mediator that is structurally linked to short pentraxins, such as C-reactive protein (CRP) and serum amyloid P component. PTX3 is produced by a variety of tissues and cells, including vascular endothelial cells and macrophages. Because of its extrahepatic synthesis (in contrast to CRP), the PTX3 level is believed to be a true independent indicator of disease activity because PTX3 is produced at sites of inflammation and is intimately linked to endothelial dysfunction. PTX3 also has key functions in innate immunity and has been identified in atherosclerotic lesions. Previously, PTX3 was associated with myocyte damage in myocardial infarction (MI), mortality after MI, and unstable angina. Because PTX3 release is likely a specific response to vascular damage, PTX3 levels may provide more explicit information on development and progression of atherosclerosis than nonspecific markers like CRP and interleukin-6. Asymmetric dimethylarginine (ADMA) is a naturally occurring component of human blood plasma. More than one decade ago ADMA was first reported to exert biological effects by inhibiting nitric oxide synthesis. Many researchers today agree that ADMA may play a prominent role in the pathogenesis and in the progression of cardiovascular diseases. In this study PTX3 and ADMA levels investigated of valsartan and nebivolol’s effect on newly diagnosed hypertensive patients.