Abstract

The storage and voluntary micturition of urine are the primary physiological functions of the normal urinary bladder. Estrogen seemingly plays an important role in the function of the lower urinary tract; however the effect of estrogen on the bladder is still unclear. Estrogen deficiency after menopause has been shown to cause atrophic changes within the urogenital tract, and is associated with urinary tract symptoms of dysfunction, such as incontinence, recurrent infection, and increased frequency and urgency. The purpose of this study was to test the following hypothesis 1) that age related decreases in estrogen in females are associated with a decrease in nitric oxide (NO) sensitivity of the bladder smooth muscle, and 2) that estrogen replacement therapy (ERT) will restore the bladder’s sensitivity to NO. NO sensitivity was assessed in female adult cats in control, sham, ovariectomized, and ovariectomized plus ERT (7 days or 28 days). In these conditions an NO donor, 3-morpholinosydnonimine (SIN-1) was used to assess the NO sensitivity of the bladder. The time to onset and frequency of spontaneous contractions and micturition volume threshold (MVT) were measured and compared among the various experimental groups. Results demonstrated that the depletion of estrogen, caused by the ovariectomy, reversed the effect of NO seen in controls. The reverse effect resulted in a shorter onset time to spontaneous contractions and to MVT. Continuous estrogen replacement (28 day, but not 7 day) returned the bladder response to SIN-1 towards control, suggesting that ERT (28 day) restored lower urinary tract function.

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