Effect of angiotensin-converting enzyme inhibition and angiotensin II type 1 receptor blockade on apoptotic changes in contralateral testis following unilateral testicular torsion

In this experimental study, our aim was to determine whether angiotensin-converting enzyme (ACE) inhibition and angiotensin II type 1 (AT1) receptor blockade affect the apoptotic changes in contralateral testis following unilateral testicular torsion (UTT). Study groups consisted of 30 adult male Wistar rats. The rats were randomly separated into five groups. Group 1 was maintained as control without manipulation. Group 2 underwent the sham operation. Torsion was created by rotating the left testis 720 clockwise for 4 h and maintained by fixing the testis to the scrotum in the other groups. Group 3 underwent torsion and detorsion, with saline administration after detorsion. In group 4, the same surgical procedure was done as in the detorsion group, but AT1 receptor blocker (losartan 30 mg/kg) was injected intraperitoneally for 60 min before detorsion. In group 5, the same surgical procedure was done as in the detorsion group, but ACE inhibitor (lisinopril 50 mg/kg) was injected intraperitoneally for 60 min before detorsion. Bilateral testes were removed from each rat 24 h after surgery. Apoptosis was assessed in paraffin-embedded sections stained for TUNEL method. Reticulum staining was performed to evaluate the extracellular changes semiquantitatively. Testicular biopsy score counts were performed on these sections according to Johnsen. The mean apoptotic scores of group 1, group 2 and group 3 were significantly higher than that of the other groups. There was no difference between the apoptotic scores of groups 1, 2, 4 and 5. Reticulum stain was increased in group 3 as compared to other groups. The mean Johnsen biopsy score of group 3 was significantly lower than that of the other groups. ACE inhibition and AT1 receptor blockade reduced the tubular damage and apoptosis in the contralateral testes after UTT. The beneficial effect of these drugs may arise from inhibition of ischemic process resulting from increased sympathetic activity and elimination of insults subsequent to dysregulation of RAS. These results suggest that ACE inhibitors and AT1 receptor blockers may be of potential value in patients with UTT.