Endothelial dysfunction at refractory arterial hypertension

Abstract

Objective: to assess endothelial dysfunction and its genetic and immunological mechanisms in patients with refractory arterial hypertension. Materials and Methods: at this study 42 patients (30 men (71.4%) and 12 women (28.6%)) with refractory arterial hypertension of III severity were examined. The patient's average age was 59.4 ± 1.12 years. The metabolic stability of the endothelium was assessed by a pharmacological test for endothelium-dependent vasodilation. Immunological analysis was carried out by the enzyme-linked immunosorbent assay. Genetic testing was performed on genomic DNA taken from whole venous blood samples. Results: in 33.3% of cases, a loss of metabolic resistance of endothelial cells to oxidative stress products was recorded. An imbalance was revealed between cytokines of a pro-inflammatory nature (tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6)) and anti-inflammatory substrates (interleukin-4, interferon-γ) in favor of the former. In patients with refractory arterial hypertension, a decrease in metabolic endothelial resistance is associated with the presence of «-174 G/C» polymorphism in the IL-6 gene and «308 G/A» in the TNF-α gene. Conclusions: in 1/3 of the examined patients with refractory arterial hypertension, there was a loss of endothelial cell resistance to the action of cytotoxic products, associated with hyperproduction of TNF-α, IL-6, as well as the presence of polymorphism «-174 G/C» in the IL-6 gene and «308 G/A» in the TNF-α gene.