Abstract

Four female baboons underwent cystometry and simultaneous urethral pressure profilometry (UPP) in a hypoestrogenic castrate state, after estrogen treatment, and after concurrent testosterone and estrogen treatment. Studies were performed under general anesthesia both before and after skeletal muscle paralysis. The results provide objective evidence that estrogen replacement enhances the urethral sphincter mechanism in the castrate female baboon by significantly increasing the paralyzed and nonparalyzed urethral length as well as the paralyzed total UPP area and the paralyzed UPP area to maximum urethral closure pressure (MUCP). The area increases reflected both the increase in functional urethral length as well as increases in mean urethral pressure. Muscle paralysis significantly reduced MUCP in all three hormonal states. The addition of testosterone had no significant effect on the UPP measurements. These findings are discussed in light of conflicting human studies regarding objective evidence for the role of hormonal modulation of urethral function and the role of estrogen therapy for stress urinary incontinence.

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