Background. The aim was to establish the features of hemodynamic and metabolic parameters in obese patients with true and pseudo-resistant arterial hypertension (AH). Material and methods. The study included 200 patients with uncontrolled AH and obesity. Patients were initially prescribed dual antihypertensive therapy. Those patients who did not reach target blood pressure (BP) levels after 3 months on dual therapy were additionally prescribed a third antihypertensive drug. Of the 98 patients who were assigned to triple therapy, 48 patients did not reach target BP (27 patients had pseudo-resistant and 21 patients had true resistant AH). These patients were additionally prescribed a fourth antihypertensive drug (spironolactone). The effectiveness of the treatment was evaluated 6 months after the start of antihypertensive therapy. Results. After 6 months of therapy, unlike patients without resistance, individuals with resistant AH had more pronounced cardiovascular remodeling and metabolic disorders, disbalance of oxidative stress-antioxidant protection, proinflammatory activity and higher activity of the renin-angiotensin-aldosterone system. Patients with true resistance differed from pseudo-resistant patients by having significantly lower body mass index (BMI); in the absence of differences in BP levels, cardiovascular remodeling, lipid and carbohydrate profiles, patients with true resistance had significantly higher levels of aldosterone, higher activity of oxidative stress system, lower levels of general antioxidant protection, higher adiponectin levels, and lower leptin level. Conclusions. Obese patients with true resistance differed from pseudo-resistant patients by having significantly lower BMI, higher aldosterone levels, more pronounced imbalance of the system of oxidative stress-antioxidant protection and less pronounced adipokine imbalance.

Background: Hereditary component plays a significant role in the formation of insulin resistance (IR) - one of the pathogenetic links of arterial hypertension (AH) and type 2 diabetes mellitus (DM2). However, the genetic predisposition to IR can not be realized and does not manifest itself clinically in the absence of appropriate factors of the environment (excessive nutrition, low physical activity, etc.). Objective: The review summarizes the results of studies which describe the contribution of genetic polymorphism to the formation and progression of AH, DM2 and their comorbidity in various populations. Results: In many studies, it has been established that genetic polymorphism of candidate genes is influenced by the formation, course and complication of AH and DM2. According to research data, the modulating effect of polymorphism of some genetic markers of AH and DM2 on metabolism and hemodynamics has been established. The results of numerous studies have shown a higher frequency of occurrence of AH and DM2, as well as their more severe course with adverse genetic polymorphisms. At the same time, the role of genetic polymorphism in the formation of AH and DM2 differs in different populations. Conclusion: Contradictory data on the influence of gene polymorphisms on the formation of AH and DM2 in different populations, as well as a small number of studies on the combined effects of several polymorphisms on the formation of comorbidity, determine the continuation of research in this direction.

Introduction: The metabolic syndrome is one of the most discussed cross-disciplinary problems of modern medicine. Now there are various definitions and criteria of diagnostics of metabolic syndrome. The abdominal obesity is considered the main component of the metabolic syndrome, as a reflection of visceral obesity which degree is offered to be estimated on an indirect indicator – a waist circumference. Alongside with abdominal obesity, a number of classifications distinguish insulin resistance (IR) as a diagnostic criterion of metabolic syndrome. It is proved that IR is one of the pathophysiological mechanisms influencing the development and the course of arterial hypertension (AH), type 2 DM and obesity. There are two components in the development of IR: genetic (hereditary) and acquired. In spite of the fact that IR has the accurate genetic predisposition, exact genetic disorders of its appearance have not been identified yet, thus demonstrating its polygenic nature. The aim: To establish possible associations of the insulin receptor substrate-1 (IRS-1) gene polymorphism with the severity of the metabolic syndrome components in patients with arterial hypertension (AH). Materials and methods: 187 patients with AH aged 45-55 years and 30 healthy individuals. Methods: anthropometry, reactive hyperemia, color Doppler mapping, biochemical blood analysis, HOMA-insulin resistance (IR), glucose tolerance test, enzyme immunoassay, molecular genetic method. Results: Among hypertensive patients, 103 had abdominal obesity, 43 - type 2 diabetes, 131 - increased blood triglycerides, 19 - decreased high density lipoproteins, 59 -prediabetes (33 - fasting hyperglycemia and 26 - impaired glucose tolerance), 126 had IR. At the same time, hypertensive patients had the following distribution of IRS-1 genotypes: Gly/Gly - 47.9%, Gly/Arg - 42.2% and Arg/Arg - 10.7%, whereas in healthy individuals the distribution of genotypes was significantly different: Gly/Gly - 86.8% (p<0.01), Gly/ Arg - 9.9% (p<0.01) and Arg/Arg - 3.3% (p<0.05). Hypertensive patients with Arg/Arg and Gly/Arg genotypes had significantly higher HOMA-IR (p<0.01), glucose, insulin and triglycerides levels (p<0.05), than in Gly/Gly genotype. At the same time, body mass index, waist circumference, blood pressure, adiponectin, HDL, interleukin-6, C-reactive protein, degree of endothelium-dependent vasodilation, as well as the frequency of occurrence of impaired glucose tolerance did not significantly differ in IRS-1 genotypes. Conclusions: in hypertensive patients, the genetic polymorphism of IRS-1 gene is associated with such components of the metabolic syndrome as hypertriglyceridemia and fasting hyperglycemia; it is not associated with proinflammatory state, endothelial dysfunction, dysglycemia, an increase in waist circumference and decrease in HDL.

Relevance. The activation of free radical oxidative processes and the development of oxidative stress is one of the most important pathogenetic mechanisms of cardiovascular diseases. Active forms of oxygen can change cellular infiltration of vessels and endothelial function, having an impact on a functional condition of the adhesive molecules intercellular adhesion molecule-1 and vascular cell adhesion molecule-1. Under condition of insulin resistance (IR), the balance in the system of oxidative stress ­–­ antioxidant protection is disturbed, the result of which is insufficient resistance to the damaging effect of the LPO products. The aim of the study was to assess the dependence of the activity of the system of oxidative stress – antioxidant protection on insulin resistance (IR) in patients with comorbidity of arterial hypertension and obesity. We examined 200 patients with hypertension and class I–II obesity. The patients were divided into two groups depending on IR: the first group included 80 patients without IR and the second group – 120 patients with IR. As the result of the study, it was established that the presence of IR affects the activity of the system of oxidative stress – antioxidant protection in comorbidity of hypertension and obesity. In the presence of IR, patients with hypertension and concomitant obesity have significantly higher levels of indicators of the system of oxidative stress (malondialdehyde (MDA) and diene conjugates (DC)) compared with patients without IR. In patients with comorbidity of hypertension and obesity, HOMA-IR directly correlated with the indicators of the oxidative stress system (MDA and DC) and inversely correlated with the indicator of total antioxidant protection. In hypertensive patients with obesity and no IR, an increase in HOMA-IR was associated with a decrease in total antioxidant protection, and in patients with IR, an increase in HOMA-IR was associated with an increase in MDA and DC, as well as a decrease in total antioxidant protection.

Background: The aim was to establish the features of metabolic disorders and the state of the renin-angiotensin-aldosterone system (RAAS) in obese patients with true and pseudo-resistant arterial hypertension (AH).Material and Methods: The study included 200 patients with uncontrolled AH and obesity. Patients were initially prescribed dual antihypertensive therapy. Those patients who did not reach target blood pressure (BP) levels after 3 months on dual therapy were additionally assigned a third antihypertensive drug. Of the 98 patients who were assigned triple therapy, 48 patients did not reach target BP (27 patients had pseudo-resistant and 21 patients had true resistant AH). These patients were additionally prescribed a fourth antihypertensive drug (spironolactone). The effectiveness of the treatment was evaluated 6 months after the start of antihypertensive therapy.Results: After 6 months of therapy, unlike patients without resistance, individuals with resistant AH differed more pronounced metabolic disorders and higher activity of the RAAS. Patients with true resistance differed from pseudo-resistant patients with significantly lower body mass index (BMI); in the absence of differences in BP levels, lipid and carbohydrate profiles, patients with true resistance had significantly higher levels of aldosterone, higher adiponectin levels, and lower leptin level.Conclusions: Obese patients with true resistance differed from pseudo-resistant patients with significantly lower BMI, higher aldosterone levels, and less pronounced adipokines imbalance.