Effects of nifedipine on bladder overactivity in rats with cerebral infarction

Purpose: Our objective was to evaluate the effect of the calcium (Ca2+) cha nnel blocking agent nifedipine on bladder overactivity induced by middle ce rebral artery (MCA) occlusion and determine its site of action. Materials and Methods: Seven days after implantation of a bladder catheter, a cannula for intracerebroventricular and intrathecal administration was i mplanted and the left MCA was occluded with 4-0 monofilament nylon thread i n male SD rats. Twenty-four hours after the induction of cerebral ischemia, saline was infused into the bladder at a constant rate (200 mu L/min.) and cystometrogram was measured in conscious state. Nifedipine was administere d intracerebroventricularly (5 mu L) or intrathecally (20 mu L) at graded d oses (0.15 ng.-0.15 mu g., 0.15 mu g. -1.5 mu g., respectively). Results: Bladder capacity in conscious rats was significantly reduced after the left MCA occlusion. Intracerebroventricular administration of nifedipi ne significantly increased bladder capacity in cerebral infarcted rats but not in sham operated rats. Furthermore there was no significant difference in bladder capacity between before and after intrathecal administration of nifedipine in cerebral infarcted rats. Conclusion: These results show that Ca2+ channel blocking agents can operat e especially on the supraspinal central nervous system rather than on the s pinal system in rats with neurogenic bladder overactivity following: cerebr al infarction.