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entire tissue. RESULTS: We found comparable levels of AR expression among testosterone supplemented and non-castrated rats both in the urethroplasty group (T-supplemented vs. non-castrated rats: 4.2% vs 4.8%, p[0.22) and non-surgical group (5.2% vs 4.5%, p[0.14) with virtually absent AR expression in castrated animals that did not receive T. Similarly, TIE-2 was only expressed in the presence of T, with significantly increased expression in response to surgery (Tsupplemented rats: 0.7% for the urethroplasty rats vs. 0.2% in the control group, p<0.01; non-castrated rats: 0.9% vs. 0.4%, p<0.01). An increase in vascularity following surgery was seen only in the androgen-exposed rats (T-supplemented rats: 10.8% for the urethroplasty rats vs. 8.9%, p<0.01; non-castrated rats: 8.2% vs 5.9%, p<0.01), with decreased vascularity following surgery in castrated rats (2.8% for the urethroplasty group vs 3.6%, p<0.01). AR expression, TIE-2, and vascularity were positively correlated with each other (AR vs TIE-2: r[0.511, p<0.01; AR vs CD31: r[0.36, p<0.01; TIE-2 vs CD31: r[0.37, p<0.001). CONCLUSIONS: Presence of testosterone was associated with increased AR and TIE-2 expression and resulted in increased periurethral vascularity. This suggests a mechanistic relationship between AR and TIE-2 and subsequent angiogenesis, and demonstrates that testosterone re-supplementation mitigates the effects seen in hypogonadal rats. This provides a basis for testosterone supplementation in hypogonadal men in order to reverse the effects of hypogonadism on the urethra.