Effects of Olmesartan on Endothelial Function

Abstract

It is well established that a functional endothelium contributes to maintain cardiovascular homeostasis mainly through the activity of endothelium-derived nitric oxide (NO). However, in the presence of proatherogenic risk factors including hypertension, diabetes mellitus and hypercholesterolaemia, the bioavailability of NO is reduced. This condition is defined as endothelial dysfunction and characterised by vasoconstriction, platelet aggregation, leucocyte adhesion and smooth muscle cell proliferation. A reduced availability of NO is mainly due to an increase in reactive oxygen species (ROS) production, which is responsible for NO breakdown. A large body of evidence indicates that, especially under pathological conditions, the activity of the renin-angiotensin system (RAS) is associated with angiotensin II (Ang II)-mediated ROS production, thus unbalancing endothelial function and leading to progressive vascular disease. The action of RAS is mostly linked to the downstream effects of the binding with the Ang II subtype 1 receptors (AT1). Therefore, selective RAS blockade with angiotensin receptor blockers (ARBs) is able to restore endothelial function in patients with cardiovascular risk factors. Olmesartan, an effective ARB, beyond its blood-pressure lowering effect, has been reported to affect the redox state of the vessel wall by restoring NO availability under different pathological conditions. Furthermore, it has been described that olmesartan exerts anti-inflammatory effects and increases endothelial progenitor cells. This article reviews the evidence linking olmesartan to vascular endothelial protection and examines the possibility that this effect translates to beneficial clinical properties of this ARB.