Essential hypertension (EH) is diagnosed in 90 % of people suffering from arterial hypertension (HTN). Along with drug therapy, renal denervation (RD) is used in clinical practice to reduce blood pressure (BP) in EH. In experimental studies, hypertension in SHR rats is a model of EH.
The aim of the work is to study, using a meta-analysis, the effect of RD on BP in SHR rats and its dependence on the stage of EH, initial BP, “white coat syndrome”, diet, presence of renal failure, and the method of the procedure.
Materials and methods. For the meta-analysis, 55 studies were selected that presented the level of BP in SHR rats after RD. In 51 studies, rats with two kidneys were subjected to RD (in 8 studies, unilateral total RD was studied, in 41 studies, bilateral RD (in 3 studies, afferent nerves were removed, in 5 studies, total denervation of the kidneys was performed using the radiofrequency method, in the rest, total denervation was performed using the surgical-chemical method). In 5 publications, RD effect was studied in rats with two kidneys kept on a high-salt diet. In 4 studies, RD was performed on rats with one kidney (the second kidney was removed).
Results. Bilateral total RD (both surgical-chemical and radiofrequency) effectively reduces BP in SHR rats with both standard and high-salt diets, and slows down, but does not prevent, the development of EH. After RD changes in systolic blood pressure are –23,59 [–27,88, –19,29] mmHg (–8.4 [–16.8, –6.4] %), changes in diastolic blood pressure are –19.96 [–23.74, –16.19] mmHg (–12.14 [–17.69, –6.15] %). In addition, bilateral total RD reduces the activity of the renin-angiotensin system and the level of norepinephrine. The observed antihypertensive effect of RD is approximately 2 times lower with telemetric recording of BP than with manual measurement on the tail artery, which indicates a decrease in the “white coat” syndrome after RD. With preservation of both kidneys, unilateral RD does not cause a decrease in BP.
Conclusion. Renal nerves make a significant contribution to the maintenance of EH, affecting the level of BP both at rest and under emotional stress. However, additional studies are required to resolve the issue of the role of afferentation from the kidneys in maintaining EH.

Angiotensin converting enzyme (ACE) is a key enzyme of the renin-angiotensin- aldosterone system. It plays an important role in the early prognosis, diagnosis and treatment of diseases of the cardiovascular system (CVS), kidneys, and COVID‑19. Among the factors determining the ACE level, genetic factors play an important role. Understanding the role of specific genetic determinants associated with ACE levels is important, as these genetic determinants can be potentially used as markers of high ACE levels and, accordingly, markers of high risk of developing ACE-associated diseases.
Objective. To study the genetic determinants of ACE levels/activity using data genome-wide association search (GWAS).
Design and methods. A search for publications was performed in the GWAS catalog for the period from 2010 to 2024 using the keywords: angiotensin-converting enzyme, ACE.
Results. To date, 7 GWAS studies have been carried out, resulting in identification of 14 polymorphic loci associated with the level / activity of ACE. Among them, the largest number of SNPs is located in two regions of the genome — 17q23.3 (8 SNPs) and 9q34.2 (4 SNPs). Out of these, 79 % (11 SNPs) exhibit pronounced pleiotropic effects and are GWAS-significant in relation to indicators of lipid and carbohydrate metabolism, immune status, are associated with the functional activity of the liver and kidneys, blood pressure levels. These polymorphisms are associated with a number of diseases: CVS, COVID‑19, Alzheimer’s disease, venous thromboembolism. According to GWAS data, the most pronounced pleiotropic effects are exhibited by polymorphisms: rs507666, rs495828, rs8176746 of the ABO gene (9q34.2). According to genome-wide studies with all 14 loci associated with the level / activity of ACE, polymorphisms (more than 60 SNPs) are in linkage disequilibrium, which are associated with various numerous traits associated with lipid / carbohydrate metabolism, immune / vascular reactions, functional state of the liver and kidneys, intercellular interactions, coagulation / anticoagulation system, etc., as well as with cardiovascular diseases, type 2 diabetes mellitus, COVID‑19, etc.
Conclusions. The level / activity of ACE is genetically determined by polymorphisms of predominantly genome regions 17q23.3 and 9q34.2, which exhibit pronounced pleiotropic phenotypic effects.

Cardiovascular diseases are the main cause of disability and mortality in the elderly population in developed countries. At the same time, population-based studies have shown that aging remains the most significant risk factor for cardiovascular pathology. Existing geroprotection strategies have not shown high efficiency. At the same time, the mechanisms of the negative impact of known risk factors (such as hypertension, obesity, metabolic disorders) are largely identical to the processes of cardiovascular aging.
Pathophysiological processes associated with aging include oxidative stress and mitochondrial dysfunction, impaired autophagy and increased apoptosis, telomere dysfunction, meta-inflammation and fibrosis. They are interconnected and are potentiated by the presence of hypertension and obesity, aggravating cardiovascular aging and provoking atherogenesis.
Understanding the key common links in the pathogenesis of these processes will help determine the direction of developing more effective strategies for geroprotection and prevention of cardiovascular pathology.

Relevance. Microalbuminuria (MAU) is a symptom diagnosed in kidney pathology, cardiovascular and other diseases. The study of the processes of development and progression of MAU will bring closer the solution of problems of nephrology, cardiology and pathological cardiorenal relationships.
Objective. To study the development t and progression of MAU.
Design and methods. Using the data from 6‑year follow-up of 22 clinical and anamnestic indicators of initially healthy 7,959 men (workers of locomotive crews) 18–66 years old, found out the origin of MAU and the progression of this pathological symptom. We used a confusion matrix, a multivariate regression model, relative risk assessment, Kaplan-Meier models and Cox proportional hazards model.
Results. MAU was determined to be due to arterial hypertension, excessive alcohol consumption, dyslipidemia, family history of early cardiovascular disease, I–II degree retinopathy, and smoking. In our analyses, these predictors showed statistical heterogeneity. Thus, specific characteristics of the predictors were established that can be used for their ultrastructural or biochemical identification at the cellular level and identification of their damage effect.
Conclusions. The course of endothelial dysfunction under the influence of MAU predictors varies considerably and depends on the effect of a particular factor, a set of predictors or all predictors taken together when they are involved simultaneously. These data show the need to find out ultrastructural and biochemical specific markers and their quantitative values of renal endothelial dysfunctions occurring under the influence of MAU predictors, during the development and progression of this pathological symptom in order to restore the normal function of the endothelial cell and the affected organ, as a whole as long, as there is still room for therapeutic efforts.

Background. Studying the genetic profile of patients with familial hypercholesterolemia (FH) and their phenotypic characteristics may contribute to a better understanding of the pathogenesis of the disease.
Objective. Evaluation of the genetic profile of patients with severe FH phenotype and study of the phenotype of patients with variants of uncertain significance.
Design and methods. The study included patients over 18 years of age with ≥ 7 points on the Dutch Lipid Clinical Network Criteria (DLCN) score from the register of the Centre for Atherosclerosis and Lipid Metabolism Disorders of the Almazov National Medical Research Centre. Clinical and anamnestic data were collected, and molecular genetic testing was performed to identify variants in candidate genes responsible for the development of FH.
Results. Of 127 patients (mean age 45,2 ± 12,8 years, 61,6 % women), molecular genetic analysis identified a positive diagnosis of FH in 61,4 % with a predominant presence of pathogenic variants in the LDLR gene (90,6 %) and the most frequent type II c.1202T>A p.Leu401His. Among patients with variants of uncertain significance (18,1 %) tendon xanthomas and lipoid arc of the cornea were detected in 6,7 % and 20,0 %, respectively. The mean LDL–C level before treatment was 7,7 ± 1,7 mmol/L. Variants of uncertain significance were verified mainly in low-density lipoprotein cholesterol (35,9 %) and APOB (28,2 %) genes. Three patients from the study sample are carriers of variants in two FH genes: c.*653G>A in LDLR with c.11788+16C>T in APOB; c.1465T>A in LDLR with c.*25C>T in APOE; c.817+6C>T in LDLR with c.2068–4T>A in APOB.
Conclusions. The genetic profile of patients with FH is represented by various mutation variants in a number of known genes, the presence of variants of uncertain significance in LDLR and APOB genes indicates the complex genetic nature of the disease, indicating the need for further study of their role.

Rare vasoreactive test (VRT) performance limits the effective and cheap calcium channel blocker (CCB) therapy in potential long-term vasoresponders patients with idiopathic pulmonary arterial hypertension (PAH). Long-term vasoresponders exhibit the unique (5–7 %) idiopathic PAH population with the highest survival. We presented the clinical case of a young idiopathic PAH with positive VRT and a significant advantage of CCB therapy over PAH-specific therapy. Pulmonary artery pressure and exercise tolerance normalization, complete reverse right heart remodeling were achieved on CCB therapy. Our case emphasized the importance of careful identification of VRT positive idiopathic PAH patients and the meticulous follow-up during CCB treatment.

The paper has been written in memory of professor of Pavlov First State Medical University of St. Petersburg Yanina Vladimirovna Blagosklonnaya. Presented are her most famous investigations, which enriched Russian and the world science.