Arterial hypertension is a concomitant disease in type 2 diabetes and the coexistence of both conditions increases the risk of microvascular and macrovascular complications in patients, as well as leads to a threefold increase in the risk of other cardiovascular diseases.

Aim. Identify quantitative distribution patterns of Bcl-2, p53 and c-Kit proteins and the magnitude of their expression in endocrinocytes of pancreatic islets in SHR rats with hereditary arterial hypertension.

Materials and methods. The study was conducted on 10 white Wistar rats and 10 SHR rats with hereditary arterial hypertension. Insulin, glucagon, c-Kit, Bcl-2 and p53 proteins were detected by immunofluorescence using antibodies produced by Santa Cruz Biotecnology (USA). The immunofluorescence reaction was studied using an AxioImager-M2 fluorescence microscope (Carl Zeiss, Germany) equipped with an AxioCam-5HRm camera (Carl Zeiss, Germany), using 38NE and 43NE high emission light filters (Carl Zeiss, Germany).

Results. A distinctive feature of the organization of pancreatic islets in hypertensive SHR rats was characterised by a 30 % (p < 0.05) decrease in the average area of pancreatic islets, a 14 % (p < 0.001) decrease in the number of beta cells in them, combined with an 18 % (p < 0.001) increase in the number of alpha endocrinocytes compared to normotensive Wistar animals. At the same time, insulin concentration in beta-cells of hypertensive animals was decreased by about 20 % (p < 0.001), and glucagon concentration in alpha-cells was increased by 36 % (p < 0.001). Examination of immunoreactivity to Bcl-2, p53 and c-Kit proteins in normotensive and hypertensive rats showed patterns of high and low expression in endocrinocytes of pancreatic islets. The present study shows that SHR rats develop diverse changes in the functional state of endocrine cells of the pancreas, based on which several pathogenetic aspects can be suggested to explain the remodelling of pancreatic islets in hereditary hypertension: a decrease in the number of beta cells expressing Bcl-2 protein reduces their anti-apoptotic potential and thus facilitates the formation of pro-apoptotic proteins of the BCL-2 family that activate the mitochondrial pathway of apoptosis However, against the background of a decreasing population of beta-endocrinocytes in the pancreas, such a mechanism should be regarded as ineffective.

Conclusions. Formation of hereditary hypertension in SHR rats leads to a reduction in the population of beta-cells in the pancreatic islets, a decrease in insulin concentration in them and an increase in the number of alpha-endocrinocytes. In the beta-cells of hypertensive SHR rats, the expression of proliferation factor c-Kit protein increases, the expression of the anti-apoptotic protein Bcl-2 decreases and the intracellular concentration of pro-apoptotic protein p53 remains at the level of normotensive animals. In alpha-cells of hypertensive SHR rats, the expression of c-Kit protein is suppressed against the background of the increase in the total content of pro-apoptotic protein p53 in islets, while the content of anti-apoptotic protein Bcl-2 in islets remains at the level of normotensive animals.