Correlation of vasoactive and neuroendocrine mechanisms with the state of antioxidant defense in patients with arterial hypertension

Abstract

Introduction. Antioxidants deficiency with excess of endoperoxides leads to damage of intracellular structures, aggravating the course of most diseases, including cardiovascular pathology. Given the important role of antioxidants in the regulation of physiological processes in cells, the aim of this research was to study the effect of the antioxidant status of blood serum on the expression of pro-inflammatory and vasoactive molecules by blood cells, as well as markers of the metabolic syndrome in the aspect of clarifying possible mechanisms of the pathogenesis of arterial hypertension (AH). Materials and methods. As part of the cohort study, 60 patients of both sexes with hypertension from 45 to 55 years and 15 practically healthy individuals were examined. During the study, we determined in the blood serum the concentrations of insulin, glucagon, apoA1, apoB100, nitric oxide (NO), angiotensin-II (AT-II), E-selectin, P-selectin, intercellular adhesion molecule ICAM1, vascular adhesion molecule VCAM1, VE-cadherin, epinephrine, norepinephrine, endothelin-1, vasopressin, brain natriuretic peptide (BNP), antioxidants (AOS), urokinase-type plasminogen (uPA), plasma endoperoxides (OXY), antiotensin II receptor type 1 (AT-IIR ), plasminogen inhibitor type 1 (PAI1), C-reactive protein (CRP). Results. In patients with AH an increase in the concentration of the studied adhesion molecules was revealed, with significant decrease in the level of VE-cadherin. An increase in the level of vasopressors and decrease NO production was also found. These changes were accompanied by a decrease in the level of apoA1, an increase of the levels of apoB100, insulin, BNP, uPA, PAI1, and CRP. At the same time, an increase in the level of OXY was noted, with a reduced concentration of AOS. It has been established that AOX promote decreasing of the adhesion molecules expression, as well as the production of studied vasopressors, including AT-II, endothelin-1, BNP, insulin, AROB, CRP and stimulates the level of VE-cadherin. Conclusions. AH proceed with activation of vasopressor mechanisms and sympathetic regulation, accompanied by an increase in the adhesive activity of blood cells and endothelium, as well as metabolic disorders and activation of peroxide oxidation of lipids. These changes are associated with AOS deficiency. A correlation between AOS deficiency, laboratory manifestations of a subclinical intravascular inflammatory process, increased aggregation of blood cells, dyslipidemia and dysmetabolic manifestations, as well as dysfunction of the vascular endothelium and myocardium has been established. At the same time, a high level of AOS, in comparison with its low level, is associated with a lower expression of adhesion molecules, a lower level of vasopressor molecules, especially AT-II, a decrease in the level of apoB100 and insulin, as well as a higher expression of VE-cadherin.