Background: Urethral stricture has a high recurrence rate. There is a common doctrine stating that "once a stricture, always a stricture". This fibrotic disease pathophysiology, pathologically characterized by excessive production, deposition and contraction of extracellular matrix is unknown. Angiotensin II type 1 (AT1) receptor primarily induces angiogenesis, cellular proliferation and inflammatory responses. AT1 receptors are also expressed in the fibroblasts of hypertrophic scars, whereas angiotensin II (AngII) regulates DNA synthesis in hypertrophic scar fibroblasts through a negative cross talk between AT1 and angiotensin II type 2 (AT2) receptors, which might contribute to the formation and maturation of human hypertrophic scars.
Objective: This study was conducted to determine the expression of AT1 receptors in urethral stricture tissues.
Methods: Urethral stricture tissues were collected from patients during anastomotic urethroplasty surgery. There were 24 tissue samples collected in this study with 2 samples of normal urethra for the control group. Immunohistochemistry study was performed to detect the presence of AT1 receptor expression. Data were analyzed using Mann-Whitney U test, and statistical analysis was performed with SPSS version 20.
Results: This study showed that positive staining of AT1 receptor was found in all urethral stricture tissues (n=24). A total of 8.33% patients had low intensity, 41.67% had moderate intensity and 50% had high intensity of AT1 receptors, while in the control group, 100% patients had no intensity of AT1 receptors. Using the Mann-Whitney U test, it was found that urethral stricture tissue had a higher intensity of AT1 receptors than normal urethral tissue with a p-value = 0.012.
Conclusion: The results showed that AT1 receptor had a higher intensity in the urethral stricture tissue and that AT1 receptor may play an important role in the development of urethral stricture.
Keywords: AT1 receptor; angiotensin; urethral stricture.