This paper is about a way of correction of endothelial dysfunction with the inhibitor of arginase: L-norvaline. There is an imbalance between vasoconstriction and vasodilatation factors of endothelium on the basis of endothelial dysfunction. Among vasodilatation agents, nitrogen oxide plays the basic role. Amino acid L-arginine serves as a source of molecules of nitrogen oxide in an organism. Because of the high activity of arginase enzyme which catalyzes the hydrolysis of L-arginine into ornithine and urea, the bioavailability of nitrogen oxide decreases. The inhibitors of arginase suppress the activity of the given enzyme, raising and production of nitrogen oxide, preventing the development of endothelial dysfunction. 1. Introduction The reasons and pathogenesis of cardiovascular diseases have always been the object of steadfast attention as the given pathology remains a principal cause of death rate of people. The list of the most frequent diseases of heart and vessels include ischemic illness of heart, arterial hypertension, cerebrovascular diseases. In the pathogenesis of these disorders, the basic role belongs to endothelial dysfunction [1]. Endothelial dysfunction is the first stage of development of heart and vessel illnesses. It is known that endothelium is capable of excreting factors of vasodilatation which relax smooth muscles of a vascular wall and lead to vasodilatation. On the other hand, there are endothelium factors of vasoconstriction. As a whole, on endothelial dysfunction, an imbalance between these factors production and vasoconstriction agents’ prevalence takes place [2]. In addition endothelial dysfunction, which can lead to the breakdown of the blood-brain barrier and impair cerebral autoregulation and prothrombotic changes, is believed to be important in mediating leukoaraiosis. The normal cerebral endothelium plays a crucial role in the regulation of cerebral blood flow and autoregulation and in the blood-brain barrier. In addition, in health, it presents an anticoagulant phenotype to blood. Upon stimulation by numerous agents, the endothelium undergoes changes that allow it to participate in the inflammatory response; this is known as endothelial cell activation (ECA) [3]. One of the changes of ECA is increased vascular permeability, and it is thought that the entry of serum proteins into the vascular wall and perivascular neural parenchyma may produce toxic effects [4]. Endothelial dysfunctions may also give rise to molecular events involving a shift in the O(2) and CO(2) trafficking system in the red blood cells, which will
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