Abstract
Nitric oxide (NO) is a universal regulator of different processes, including vascular tone, hemostasis ?nd apoptosis. One of the important functions of NO as a signaling molecule is determined by a high capacity for diffusion through the cell membrane to synthesize it and penetrate into target cells by controlling their metabolism ?nd realizing intercellular interactions. For the purpose of estimation in elderly persons due to for determine the effect of nitric oxide and its products on the process of subclinical inflammation and apoptosis of endothelial cells in the development of endothelial dysfunction as a target organ in arterial hypertension 66 patients of elderly age with arterial hypertension (AH) of II stage and 24 persons of similar age without cardiovascular diseases were examined. The degree of endothelial dysfunction was examined by dopplerography of brachial artery, the endotheliocytemia level was estimated by the Hladovec and Rossmann method, the concentration of nitric oxide - in the Griess reaction, the levels of C-reactive protein, primary inflammatory mediator of TNF-a, apoptosis markers and nitrotyrosine - were determined by the immune enzyme method. It has been established that the synthesis of basal nitric oxide depends on the activity of endothelial constitutive NO - synthase and maintains the tone of the vessel in a state of light relaxation. In the progression of endothelial dysfunction (ED) a number of phases were identified: a compensation phase with increased secretory activity of endothelial cells, an intermediate phase when the balance is disrupted due to changes in the secretion process of production and inactivation of endothelial factors and a decompensation phase as a result of structural and metabolic disorders of endothelium resulting in its functional failure, death and desquamation. Regulatory effect of NO on subclinical inflammation and apoptosis intensity was confirmed by its strong inverse correlation with the level of TNF-a and caspase-3. It proved the change in the NO concentration, its auto- and paracrine effect on the formation of involutive changes in the vascular wall, its regulatory effect on the processes of subclinical inflammation and apoptosis of endothelial cells in the formation of hypertension, as well as its progression during aging.
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