PECULIARITIES OF FATTY ACID PROFILE OF ERYTHROCYTE MEMBRANES IN PATIENTS WITH RESISTANT ARTERIAL HYPERTENSION

Abstract

Objective: This study aims to evaluate peculiarities of composition and level of fatty acids (FAs) in erythrocyte membranes (EM) of patients with resistant arterial hypertension (RAH) which could be applied in diagnosis of pathogenic aspects of the disease, development of new therapeutic targets. Design and method: 24 males with controlled arterial hypertension (CAH) (stage 1–2), 20 subjects with RAH (53 ± 5.7years), 22 healthy males were included into the study. The Agilent 7000B (USA) GC system was applied to study FAs composition. Results: The patients with CAH demonstrated increase in ratio of saturated, monoenoic FAs as well as decrease of polyenoic ones. Significant increase was registered in levels of C14:0, C17:0, C18:0, C20:0, C18:1 n9 (p = 0.01–0.05). We registered decrease in ratio of n6 unsaturated FAs: (C18:2, C20:4, C22:4) n6, (p = 0.01–0.05). Patients with RAH displayed increase in levels of C15:0, 16:0 FAs, oleic, midic ones (p = 0.03–0.05). The registered increased level of C20:3n9 would compensate synthesis which would take place in cases of deficit of n6, n3 polyunsaturated FAs (PUFA). Increase in ratio (C20:3/C18:1) n9 tends to evoke active synthesis of substrates for formation of prostacyclins, thromboxanes which are known to possess vasoconstrictive properties. Changes in PUFA tended to be most highly pronounced, especially in cases of n3 (C22:5, C22:6; p < 0.01). Patients with RAH demonstrated 2.1-time decrease of total n3 PUFA as compared to subjects with CAH. Increase of arachidonic acid level by up to 37.8% served as an outstanding finding in patients with RAH. That was the sign of deficit of n-3 PUFA. Disbalance in structure of n3, n6 was seen in decreased n3/n6 ratio (p < 0.01). Patients with RAH demonstrated accumulation of saturated, polyunsaturated n6 FA with deficit of n3 PUFA in EM. This speaks in favor of decrease in fluidity of cellular lipid bilayer, inhibition of binding ligands with the receptor, activity of enzymes bound with membrane, including PIEZO1,2 proteins (responsible for sensitivity to pressure). Conclusions: Increase in disorganization of lipid components of cellular membrane causes progression of hypertension with further development of resistant forms, what should be considered an important link in pathogenesis and target for therapy.