Background. The CYP11B2 gene as the main controller of aldosterone plasma activity is likely to be responsible as for the BP level as for the expression of different traits of hypertensive cardiac remodeling such as increased left ventricular mass and myocardial fibrosis. The main objective of our study was to define the differences in myocardial remodeling depending on CYP11B2 gene polymorphism. It was shown that some special techniques of echocardiography such as the assessment of inappropriate left ventricular mass and myocardial echoreflectivity proved additional information in patients with hypertensive heart disease. That's why these techniques were used for a more precise assessment of hypertensive cardiac remodeling. Material and methods. Our study involved 150 males aged 45-60 years. They were divided into three groups: Group 1-50 patients with normal BP without any echocardiographic abnormalities, Group 2-52 patients with essential hypertension without left ventricular hypertrophy, and Group 3-48 patients with essential hypertension and left ventricular hypertrophy. Results. It was found that in patients with inappropriate LVM the prevalence of CC genotype was almost twice higher than among those with appropriate LVM. On the other hand, hypertensive patients with CC genotype and LVH demonstrated higher echoreflectivity parameters. Conclusions. We assume that CC polymorphism of CYP11B2 may be an indicator of more expressed signs of hypertensive cardiac remodeling, in particular myocardial hypertrophy and myocardial fibrosis, in males with essential hypertension.

The concentrations of galectin-3 and BNP, central and systemic hemodynamics, structural and functional heart parameters in male carriers of polymorphic AT1R genes without cardiovascular pathology (n = 79) living in Podillya region were studied. Genotyping of the AT1R gene was carried out using a polymerase chain reaction. The level of galectin-3 and BNP was determined by the method of enzyme immunoassay. It was found that the A1166A genotype dominated in practically healthy men of Podilly region. Nevertheless, the level of galectin-3 and BNP in the studied population did not significantly depend on the carriage of a specific variant of the AT1R gene.

Objectives: Hypertensive heart remodeling requires the assumption of different factors, including an increase of left ventricular mass (LVM) and myocardial fibrosis. It was shown that aldosterone stimulates cardiac collagen synthesis and fibroblast proliferation. CYP11B2 is one of the genes responsible for the effects of aldosterone. Therefore, hypertensive remodeling could be partially related to the polymorphism of this gene. The purpose of this study was to assess the association of CYP11B2 polymorphism with structural remodeling by changes in geometry and myocardial density to define their role and interaction in hypertensive heart disease. Methods: The study recruited 150 men aged 45-60 with and without essential hypertension (EH), who possessed no irreversible target organ damages. Fifty of them had normal BP, 58 had EH without left ventricular hypertrophy (LVH) and 42 had EH and LVH. Each participant underwent office blood pressure measurement, echocardiography with echo-reflectivity analysis, and determination of the C-344T polymorphism of the aldosterone synthase gene CYP11B2. Results: Patients with EH and LVH differed not only by LV mass but also by larger body mass, relative wall thickness, and wider echo-reflectivity spectrum. The associations of larger end diastolic diameter with C allele, and the larger thickness of the posterior wall and interventricular septum with T allele, were revealed only in patients with EH and LVH. Conclusions: Hypertensive patients with LVH are likely to be a distinct cluster with their own genetic predisposition to hypertensive heart disease.

According to previous studies, aldosterone is responsible for myocardial remodeling and, ultimately, myocardial dysfunction. Aldosterone synthase gene (CYP11B2) as the main controller of aldosterone may be involved in the variability of renin-angiotensin-aldosterone system (RAAS) activity. Brain natriuretic peptide (BNP) is a marker for the diagnosis of chronic heart failure and it’s a contraregulatory peptide of RAAS. The aim of our study was to investigate the levels of BNP plasma concentrations in men with uncomplicated hypertension, carriers of polymorphic variants of the CYP11B2 gene. The study involved 150 men: 50 men of control group and 100 men of main group patients with hypertension of I-II stages. Each participant underwent office blood pressure measurement, echocardiography, determination of plasma levels of BNP in serum by immunoassay (ELISA) and determination of C-344T polymorphism of CYP11B2 gene in venous blood samples by PCR. Mathematical processing of obtained data was performed using standard statistical package STATISTICA 10.0. In accordance with the normal distribution, obtained results were presented as mean and standard deviation. In case of discrepancy of normal distribution a median of 25-75% of quartiles, including half of all parameter values, was given. For comparing groups by investigated parameters, the Student's t test was used for normal distribution, and in the absence of normal distribution, its non-parametric analogs were used: the Mann-Whitney or ANOVA test. It was found that male carriers of CC polymorphism of CYP11B2 gene had higher plasma concentrations of BNP and in the group of patients with essential hypertension and left ventricle hypertrophy (LVH) the representatives of this polymorphic variant of CYP11B2 gene had more severe diastolic disorders and signs of myocardial remodeling. The TT carrier of the CYP11B2 gene polymorphism was associated with excess body mass and lower BNP levels.

Widespread use of antibiotics in clinical practice leads to the development of antibiotic resistance and encourages the search for new ways of modulation of their therapeutic effect. One of the potentially successful modulators may be Hydrogen sulfide, but the mechanisms of its action require careful studies, including toxicological. The aim of the study was to study the effect of Hydrogen sulfide levels on the embryotoxicity and fetotoxicity of oral and intravaginal Clindamycin phosphate administration. The experimental study was performed on 60 pregnant female rats, which were divided into 6 experimental groups: group 1 – control group; group 2 – high level of serum Hydrogen sulfide; group 3 – Clindamycin phosphate intravaginally; group 4 – Clindamycin phosphate intravaginally with high level of serum Hydrogen sulfide; group 5 – Clindamycin phosphate orally; group 6 – Clindamycin phosphate orally with high level of serum Hydrogen sulfide. We studied the dynamics of weight gain in pregnant rats, the number of corpora lutea, the number of implantation sites in the uterus, the number of live and dead fetuses, preimplantation and postimplantation mortality, as well as the dynamics of body weight gain and mental development of offspring. Artificially increasing the serum level of Hydrogen sulfide in pregnant rats led to an increase in maternal weight gain, an increase in the weight and cranio-caudal size of embryos, as well as a decrease in the number of resorbed fetuses and postimplantation mortality. The insignificant toxic effect of high doses of oral Clindamycin phosphate was leveled in the group with elevated indices of serum Hydrogen sulfide. Rats born to females with elevated levels of serum Hydrogen sulfide showed faster rates of weight gain and normal mental development according to the “open field” test.