Purpose: Bladder hyperactivity is a frequent and embarrassing symptom of bladder outlet obstruction and often persists even after effective removal of the obstruction. It has been proposed that gap junctions be present in models of bladder overactivity including outlet obstruction. We therefore determined whether the gap junction protein connexin43 and its associated mRNA were present in normal and obstructed rat bladders. Materials and Methods: Obstruction was created in female Sprague-Dawley rats by placement of a ligature around the urethra which limited urethral opening; the ligature was omitted in controls. After 6 weeks, bladders were harvested and processed for detection of connexin43 mRNA by competitive RT-PCR or connexin43 protein by immunohistochemistry. Results: Connexin43 mRNA was present in control bladders and at least 2-fold upregulated in obstructed bladders. No connexin43 immunoreactivity was observed in control bladder smooth muscle. Connexin43 immunoreactivity between bladder smooth muscle cells was present in all obstructed bladders and presumably represents gap junctions. Conclusions: The results directly support the hypothesis that gap junctions ate upregulated in obstructed bladders due to lowered input resistance of hypertrophied myocytes. Thus, they may contribute to bladder instability by increasing intercellular electrical coupling.
|Translated title of the contribution||Increased expression of connexin43 in rat bladder outlet obstruction a possible cause of obstruction-derived bladder hyperactivity|
|Number of pages||9|
|State||Published - Sep 2002|
- Gap junctions
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