Abstract
Reduction in urinary bladder blood flow (chronic bladder ischemia or CBI) may lead to oxidative damage and bladder dysfunction. The bladder urothelium (UT) plays an important role in urinary bladder barrier function and sensory outputs, but little is known about the impact of ischemia on UT structure/function. We investigated the impact of CBI on the expression of UT (structural/sensory) proteins and distribution of nearby lamina propria IC cells (LP‐IC; integrates signals within bladder wall). Urinary bladders (UB) were removed from Sprague‐Dawley rats that underwent a balloon endothelial injury of the iliac arteries (high cholesterol diet, 8 wks) versus sham control. The following antibodies were used for immunocytochemistry, western immunoblotting or ELISA: vimentin (LP‐IC), ZO‐1 (tight junction protein), UPIII (superficial UT cells), norepinephrine (NE) and NGF (nerve growth factor). Findings of an ischemia‐induced decrease in ZO‐1 and UPIII expression suggest a defect in UT integrity while a reduction in mucosal NE suggests increased sympathetic activity. NGF may protect against neural or epithelial deficits in hypoxic or ischemic conditions, as evidenced by decreased UT‐NGF. Our findings show that ischemia‐induced changes in UT‐cell interactions (with increased number of vimentin‐positive cells) may alter sensory mechanisms thus contributing to the pathophysiology of bladder disease.
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