Morphofunctional alterations in endothelium in the pathogenesis of essential hypertension
Endothelium is a multilevel cellular structure that permeates all organs and systems of the body. A disorder of the regulation of the arterial tone underlies essential hypertension. However, its pathogenesis basis, despite intense efforts, remains unclear. The unfavorable role of emotional stress, hypodynamia, obesity and disorder of water-salt metabolism is obvious. However, the exact mechanisms and predictors of the development of arterial hypertension (HTN) are not currently defined. This opposes the prevention and detection of essential hypertension at an early stage. The investigation of endothelial function as a target and a predisposing factor for HTN development is promising and implies both scientific and applied clinical significance. Indeed, understanding of pathognomonic endothelial alterations for HTN development will clarify its pathogenesis and will help the development of the adequate treatment protocols. The review current data on the involvement of endothelial cells (EC) in the development of HTN. The role of lipid disorders in the physiological state of the endothelium is shown. The role of endothelial dysfunction in increasing production of active oxygen species and disorders in the nitric oxide metabolism is highlighted. The activity of the following enzyme is reviewed: NADPH (nicotinamide adenine dinucleotide phosphate) oxidase, cyclooxygenase, xantinoxydoreductase and endothelial NO synthase. The interaction of the endothelium and the extracellular matrix, as well as endothelium and smooth muscle cells, is also given according to the literature data. The role of ghrelin, produced by endothelium, in the regulation of vascular tone is highlighted. Methods of the EC assessment in vitro under hypoxia are presented. Based on the literature review, it is clear that the assessment of the endothelium under hypoxia is highly important, as well as the investigation of the influence of tissue and hemic hypoxia in vivo. These studies will help to establish the contribution of functional endothelial disturbances to the development of HTN.