Abstract
Aims
Estrogen is essential for physiological maintenance of the female urogenital tract. It is believed that alterations in female sex hormones play a major role in the etiology and response to urinary tract dysfunctions. In animal studies, ovariectomy (Ovx) results in smooth muscle (SM) weakness and atrophy whereas estrogen supplementation reverses these effects. Our study seeks to establish the mechanisms by which estrogen augmentation results in increased contractility.
Methods
Twenty New Zealand White female rabbits were separated into five groups of four each. Group 1 served as control, rabbits of groups 2β5 were ovariectomized, group 2 ovariectomized received no estradiol, groups 3β5 were given 17βΞ² estradiol (1 mg/kg/day) by subcutaneous slow release tablet implant for 1, 3, and 7 days, respectively, beginning 2 weeks after Ovx. At the end of the experimental period, each rabbit was anesthetized and the urinary bladder was removed for contractile, histological, and biochemical studies.
Results
Ovx resulted in significantly decreased bladder contractile function, whereas bladders tested after estradiol administration showed increased contractility. Ovx resulted in a decrease in SM/collagen ratio, whereas estrogen resulted in an increase. The estrogen receptor (ER) density significantly increased following Ovx. After 1 day of estrogen treatment, the ER density decreased significantly below control levels, but rose progressively during the estrogen treatment.
Conclusion
The present study demonstrates that estrogen supplementation mediates a βfunctional hypertrophy,β that is a hypertrophy characterized by increased contractile responses to all forms of stimulation, and an increased ratio of SM/collagen. Neurourol. Urodynam. Β© 2006 WileyβLiss, Inc.