Essential hypertension is characterized by increased peripheral vascular resistance to blood flow. The endothelium is a crucial regulator of vascular tone. Its function is impaired in patients with hypertension, with reduced vasodilation, increased vascular tone associated with a proinflammatory and prothrombotic state. Low-grade inflammation localized in vascular tissue is therefore recognized as an important contributor to the pathophysiology of hypertension, to the initiation and progression of atherosclerosis as well as to the development of cardiovascular diseases. 1. Introduction Vascular remodeling and increased peripheral vascular resistance to blood flow are common features of essential hypertension. Resistance arteries may play an important role in the development [1] and may contribute to the complications of hypertension [2]. Small decrease in the lumen of the small arteries significantly increases resistance to blood flow. Vascular tone is regulated by the endothelium, which may affect vascular function and remodeling. Endothelium is the active inner monolayer of the blood vessels, forming an interface between circulating blood and the vessel wall. It represents the largest organ in the body and plays a critical role in vascular homeostasis. Endothelial cells regulate vascular tone by releasing various contracting and relaxing factors including nitric oxide (NO), arachidonic acid metabolites, reactive oxygen species (ROS), and vasoactive peptides. Therefore, the endothelium actively regulates vascular tone and permeability, the balance between coagulation and fibrinolysis, the inflammatory activity as well as cell proliferation. Endothelial dysfunction is characterized by impaired vasomotor response (reduced vasodilation and increased endothelium-dependent contraction), cell proliferation, platelet activation, vascular permeability, and a proinflammatory and prothrombotic phenotype, including leucocyte-endothelial interactions that participate in vascular inflammation and increased adhesion and aggregation of platelets [3]. Endothelial progenitor cells (EPCs), a bone-marrow-derived population of cells which can develop into competent mature endothelial cells [4], are seen as an important determinant of endothelial function. Decreased EPCs number is associated with arterial stiffness [4] and decreased endothelial function [5]. In this regard, it has been shown that circulating EPCs are significantly reduced in hypertensive type 2 diabetic patients [4] and in salt-loaded hypertensive rats [5]. Endothelial dysfunction occurs in association
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