The purpose of this study was to determine the resultant changes in the bladder function after partial bladder outlet obstruction (BOO), with particular emphasis on the threshold voltage and on the role of NO. A total of 12 adult rabbits were used in the study. New Zealand-type rabbits were subjected to no intervention and 3 weeks duration of a partial outlet obstruction. They underwent an in vivo cystometric evaluation before and after the BOO, histological studies, bladder-strip stimulation studies using acetylcholine, electrical field stimulation, and relaxation studies using NO donor nitroprusside. Statistical significance was determined by two-way ANOVA for multiple variations and Student's t-test. Histology sections demonstrated smooth-muscle hypertrophy, hyperemia of the vessels in the wall and widely set mononuclear cell infiltration in the rabbits with partial BOO. Cystometry showed markedly decreased bladder capacities, and decrease of compliance from 4.3 +/- 1.8 to 1.6 +/- 0.3 in the obstructed group. Tissue bath studies demonstrated no meaningful change with cholinergic stimulation, increased contractility in response to electrical field stimulation, and increased threshold voltage values from 57.5 to 93.3 compared to controls. Nitroprusside did not induce relaxation of the neostigmine and acetylcholine-precontracted bladder in all animals. Hypertrophy was observed due to adaptation of the detrusor against the obstruction. During this adaptation period, bladder capacity decreases and the elasticity disappears, thus causing higher pressures with lesser volumes. In other words, compliance decreases. The neurogenic damage can be shown with increasing values of threshold voltage, and higher voltages are needed to start a contraction. Nitroprusside has no inhibitory effect on smooth-muscle tone in the rabbit bladder.