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Bladder decompensation was associated with decreased blood flow to bladder smooth muscle. Because compensated obstructed bladders with relatively normal contractile function are also hypertrophied but have normal blood flow, decreased blood flow in decompensated bladders is not simply a response to bladder hypertrophy. From this study we hypothesize that decreased blood flow to bladder smooth muscle is an etiological factor in bladder contractile dysfunction (bladder decompensation) secondary to partial outlet obstruction.

The EP1 receptor appears not to be essential for normal micturition or the mediation of bladder hypertrophy due to BOO but it seems to have a role in the development of detrusor overactivity caused by PGE2 and outlet obstruction.

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Rapamycin prevents mechanically induced hypertrophy in cardiovascular smooth muscle. In vivo mTOR inhibition may attenuate obstruction induced detrusor hypertrophy and help preserve bladder function.

Partial bladder outlet obstruction causes prominent morphological changes in the bladder wall, which leads to bladder dysfunction. In this paper, we demonstrate that polarized light imaging can be used to identify the location of obstruction induced structural changes that other imaging modalities fail to detect. We induced 2-week and 6-week partial outlet obstruction in rats, harvested obstructed bladders, then measured their retardances while distended to high pressures and compared them to controls. Our results show that the retardance of the central part of the ventral side (above the ureters) closer to the urethra can be used as a potential metric of the distending bladder obstruction.