In vitro analysis of the effect of hyperbilirubinemia on rabbit ureter and bladder

Spontaneous resolution of intrauterine pelvic dilatations after birth is an expected outcome. In nonobstructive pelvic dilatations, changes in ureteral and bladder physiology may also play a part. We aimed to demonstrate the effect of increased concentrations of bilirubin on ureteral and bladder muscles in vitro. Normal and pathologic concentrations of bilirubin (3.5×10^-7–10^-5M and 10^-4–4×10^-4M, respectively) caused no change in the basal ureter tension (343.9±29.4 mg). Normal concentrations of bilirubin caused no difference in basal bladder tension (430.2±70.2 mg), but pathologic concentrations caused a decrease of 303.8±52.9 mg. Normal and pathologic amounts of bilirubin were cumulatively applied to rabbit ureteral and bladder tissues both after reaching basal tension and when contracted with KCl (80 mM and 120 mM KCl for ureter and bladder, respectively). The cumulative addition of normal bilirubin concentrations to the ureteral tissues precontracted with KCl produced 86.4±7.2% relaxation, while the addition of pathologic bilirubin concentrations produced a relaxation of 133.9±17.4%, which was significantly higher (p=0.04). Similarly, the addition of normal concentrations of bilirubin to the bladder tissues precontracted with KCl produced a maximal relaxation of 35.3±2.2%, while pathologic concentrations produced a maximal relaxation of 53.5±3.5%, which was significantly higher (0.001). Consequently, high concentrations of bilirubin caused a mild relaxation in basal ureteral and bladder tensions, while pathologically increased concentrations led to significant relaxation in both types of precontracted tissues. We suggest that high bilirubin levels may partly but not directly contribute to the spontaneous recovery of hydronephrosis because of the relaxation effect on bladder while probably causing susceptibility to urinary tract infections because of relaxation of both ureteral and bladder tissues.