Abstract
Previous studies indicate that bladder instability in man may be associated with increased spontaneous rhythmic contractile activity. Ca(2+) influx plays a central role in smooth muscle contractions, and recent evidence suggests that steroid hormones rapidly affect Ca(2+) influx. Therefore we tested the hypothesis that estrogen and progesterone modulates spontaneous rhythmic detrusor contractions. Tissues were secured to isometric force (F) transducers in tissue baths and length-adjusted until K(+)-depolarization produced maximum contractions (F(o)). Spontaneous rhythmic contractions (SRC) were sampled before and immediately after addition of estradiol or progesterone (10(-5) M) to tissue baths. The average frequency and amplitude of SRC were, respectively, 0.156 Hz and 0.053 F/F(o) (n = 24). Estradiol caused an immediate reduction in SRC, such that by 10 min, tone, frequency and amplitude were each reduced by, respectively, 36%, 46% and 47% (n = 7, P < 0.05). However, progesterone caused an immediate weak contraction, and at steady state (10 min), progesterone increased frequency of SRC by 152% but decreased SRC amplitude by 50% (n = 10, P < 0.05). Novel therapies using unique steroids that do not interact with genomic receptors may potentially reduce bladder smooth muscle activity, thereby reducing detrusor instability.
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