Indicators of Oxidative Stress in Rat Brain Tissue Under Conditions of Prolonged Arterial Hypertension and Its Correction With Different Generations of Beta-blockers

Abstract

Background. The significant increase in the number of patients with arterial hypertension both worldwide and in our country necessitates a more detailed study of the pathogenetic features of changes that occur in target organs, including the brain, in conditions of prolonged elevated blood pressure and against the background of its correction with beta-blockers of different generations. Objective. The aim of the study was to examine oxidative stress indicators in brain homogenates of animals with arterial hypertension and to determine the effect of long-term correction with different generations of beta-blockers on the state of pro- and antioxidant components of OS. Methods. One intact and four groups of experimental animals were studied. Experimental animals with spontaneous arterial hypertension were administered propranolol, carvedilol, and hypertril in therapeutic doses. The oxidative stress indicators (oxidative modification of proteins markers (aldehyde dinitrophenylhydrazones and carboxyphenylhydrazones) and content of reduced glutathione, and the activity of Superoxide dismutase, Glutathione peroxidase) in animal brain homogenates were biochemically studied. Results. It was established that prolonged arterial hypertension is accompanied by a deterioration in the state of antioxidant systems. Correction of high blood pressure with propranolol does not significantly affect the state of oxidative stress indicators. Carvedilol has a moderate antioxidant effect, while hypertril has a powerful antioxidant effect, which is manifested in a decrease in oxidative modification of proteins markers, and increased of antioxidant system markers content. Conclusions. Long-term administration of Propranolol stabilizes arterial pressure but does not alleviate oxidative stress in the brain, evidenced by sustained high levels of OMP markers (ADPH and CPH) and suppressed antioxidant defense (SOD, GSH, GPx). Carvedilol exerts a moderate antioxidant effect by lowering CPH levels but fails to significantly restore the activity of key antioxidant enzymes (SOD, GPx) or reduced glutathione levels. Hypertril exhibits a potent dual effect, providing both antihypertensive control and robust antioxidant neuroprotection. Its mechanism involves the significant reduction of OMP markers (ADPH and CPH) and the restoration of the antioxidant defense system (SOD, GSH, GPx).