Marker profile of myocardial remodeling in different etiopathogenetic forms of arterial hypertension in the experiment

The aim was to determine the morphodensitometric parameters of cardiomyocytes and features of the marker profile of remodeling in the left ventricular myocardium of rats with experimental hypertension of different etiopathogenetic forms. Materials and methods. The experiment was conducted on 20 male Wistar rats and 10 SHR which were divided into two groups of 10 animals each: the 1st –control; the 2nd – rats of the SHR line (EAH); the 3rd – 10 male Wistar rats with endocrine-salt arterial hypertension. Systolic and diastolic BP levels were measured in all the rats using the system of non-invasive arterial pressure measurement BP-2000. The objects of the study were myocardial sections in which the content of immunoreactive material to remodeling markers (cardiotrophin-1, titin, collagen type I, annexin V) was determined by the immunofluorescent method, titin / collagen ratio was calculated, the average linear size of cardiomyocyte nuclei, their density, RNA concentrations in the nucleus and cytoplasm were determined by morphodensitometric method. Results. Arterial hypertension, regardless of its etiopathogenetic form, is characterized by an increase in the number of cardiomyocyte nuclei with an increase in their size, decrease in the density and decrease in their RNA concentration against increase in the cytoplasm. In rats with EAH, the content of cardiotrophin-1 was higher than the control by 27 %, and in ESAH by 80 %. Titin levels were 12% higher in EAH and 46 % in ESAH. The collagen type I content of EAH was higher than the control by 49 %, while in the group with ESAH by 68 %. EAH rats had a higher annexin V content by 58 %, while ESAH – 64 %. The ratio of the content of titin and type I collagen in control rats was 1.01, in rats with EAH decreased to 0.76, while in rats ESAH it was 1.3. Conclusions. The formation of arterial hypertension, regardless of its etiopathogenetic form, leads to the development of pathological myocardial remodeling, as indicated by increased heart mass and specific gravity, changes in the cytoarchitectonics of cardiomyocytes, the development of polymorphism of their nuclei with increasing size against increasing of its number with nuclear dysfunction. The marker profile of myocardial remodeling in rats with essential hypertension is characterized by a moderate increase in cardiotrophin-1 and titin, with a significant increase in collagen type I and annexin V, which in combination with a low ratio of titin / collagen type indic