Acute bladder distension results in pressure ischemia, subsequent reperfusion injury, and ultimately damage to the detrusor. We hypothesize that changes in pressure may be a key factor to damage resulting from over-distension and developed a pressure-guided distension model to evaluate cystometric changes. Three groups of adult female Sprague Dawley rats (250 g) were used: a sham distended control group, a 3-day (3D) and 7-day (7D) follow-up group after pressure-guided distension. Under pentobarbital anesthesia, the urethra was clamped and saline was infused (0.04 mL/min) under continuous intravesical pressure monitoring. After reaching 120 cmH 2 O pressure, infusion was stopped and clamping was maintained for 30 minutes. For sham distension, all procedures except the saline infusion were done. There were no bladder ruptures during distension. Distension volumes needed to achieve the fixed pressure were variable (1.68–2.90 mL), but mean distension volumes were similar between the 3D and 7D groups (2.1 ± 0.1 mL vs. 2.2 ± 0.3 mL). After distension, maximal cystometric capacity and residual urine volume were increased at both time points. Voiding efficiencies were decreased significantly in both the 3D and 7D groups (p < 0.05) compared to controls. Maximal vesical pressure and bladder compliance showed no change before and after distension Our pressure-guided distension model exhibits cystometric characteristics of bladder decompensation. This model for the underactive bladder™ (UAB) may prove useful to further the development of targeted UAB™ treatments.