Effects of chronic treatment with vardenafil,a phosphodiesterase 5 inhibitor,on female rat bladder in a partial bladder outlet obstruction model

OBJECTIVES

To investigate whether vardenafil, a phosphodiesterase 5 (PDE‐5) inhibitor, would protect the bladder from decompensatory changes in a 4‐week rat bladder outlet obstruction (BOO) model, as evidence has been accumulating that PDE‐5 inhibitors improve lower urinary tract symptoms (LUTS) in patients with benign prostatic hyperplasia (BPH).

MATERIALS AND METHODS

In all, 50 12‐week‐old female Sprague‐Dawley rats were divided into five equal groups; group 1, sham operated vehicle control rats; group 2, BOO vehicle rats; group 3–5, BOO rats given oral vardenafil at 5, 20, 80 mg/L, respectively. Vardenafil was given in drinking water from the day of surgery. At 4‐weeks after the introduction of BOO, vardenafil was washed‐out by giving water for 24–48 h, and then the bladder was excised and dissected into four longitudinal strips for isometric organ‐bath assay. Contractile responses of bladder strips to electrical field stimulation (EFS), carbachol and KCl was determined for each group.

RESULTS

BOO induced a significant increase in bladder weight in group 2 compared with group 1. Bladder weights of groups 3–5 were not significantly different from that of group 2. The contractile forces in response to EFS, carbachol and KCl in group 2 were 30.7–51.7% of those in group 1. Vardenafil treatment in groups 3–5 generally did not block the BOO‐induced reduction of contractile force in the bladder strips. However, treatment with a high dose of vardenafil resulted in a significant increase in the contractile response to carbachol (78.4% group 5 vs 51.7% group 2).

CONCLUSION

Chronic treatment with a high dose of vardenafil protected the rat bladder from BOO‐induced contractile dysfunction to carbachol.