Background: Transforming growth factor-β1 (TGF-β1) and basic fibroblast growth factor (bFGF) are the two most important growth factors that have been found. Previous studies have indicated that the above two factors play an important role in the physiological growth, response to injury and the following fibrous proliferation of the bladder. Therefore, they may be related to the detrusor underactivity due to bladder outlet obstruction (BOO). The aim of this study is to investigate the relationship between them. Materials and Methods: 29 evaluable Wistar rats were divided into three groups: control group, BOO 2 weeks group and BOO 6 weeks group. After successful models, we measured excised bladder mass, detrusor contraction force (DCF) in vitro stimulated by carbachol of four different concentrations (10–5, 10–4, 10–3 and 10–2 mM). Simultaneously, the expression of TGF-β1 mRNA and bFGF mRNA in detrusor specimens was detected by reverse transcription polymerase chain reaction (RT-PCR) analysis. Additionally, we analyzed the correlation between DCF and the detrusor mRNA expression of the two factors to determine whether they are associated with the detrusor contraction response when BOO occurs. Results: Bladder mass increased steadily and significantly with the progression of the BOO. While at the point of 10–4 and 10–3 mM carbachol concentration, DCF in the BOO 2 weeks group was higher, no significant differences were found at the point of 10–5 and 10–2 mM carbachol concentration when compared to the control group. DCF was found to be significantly lower in the BOO 6 weeks group than in the BOO 2 weeks group and control group at all points of carbachol concentration. TGF-β1 mRNA expression of the detrusor was found to be higher only in BOO 6 weeks. However, there was a steady and significant increase of bFGF mRNA expression with the aggravation of BOO. Correlation analysis demonstrated that there was a significant moderate negative correlation between DCF in vitro and the level of TGF-β1 mRNA. Meanwhile, a significant high negative correlation was acquired between the DCF and bFGF mRNA level. Conclusion: DCF in the severe BOO group is remarkably impaired. There is a sustained rise of bFGF mRNA expression in detrusor with the progression of BOO, but TGF-β1 mRNA expression increase becomes evident only in the decompensation stage. Significant negative correlations are found between DCF in vivo and the expression of TGF-β1 mRNA, bFGF mRNA. Additionally, DCF correlates negatively with the bladder mass statistically after BOO.

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